74 results on '"Wang Rong"'
Search Results
2. PBA alleviates cadmium-induced mouse spermatogonia apoptosis by suppressing endoplasmic reticulum stress.
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Wang, Rong, Li, Mengyuan, Wu, Zhen, Gong, Wenjing, Zhang, Mingming, Liu, Yehao, Yao, Yuyou, and Ji, Yanli
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APOPTOSIS , *ENDOPLASMIC reticulum , *GENE expression , *PROTEIN expression , *MICE , *FLOW cytometry , *GERM cells - Abstract
Endoplasmic reticulum (ER) stress mediates Cd-caused germ cell apoptosis in testis. The effects of 4-phenylbutyric acid (PBA), a classical chaperone, were investigated on Cd-induced apoptosis in mouse GC-1 spermatogonia cells. The cells were pretreated with PBA before Cd exposure. TUNEL and flow cytometry assays were applied to determine apoptosis. Some key biomarkers of ER stress were analyzed using RT-PCR and western blot. as expected, the apoptotic cells exposed to Cd apparently increased. The mRNA and protein expression levels of GRP78 and ATF6α, were elevated in the Cd groups. Additional experiments displayed that Cd notably increased IRE1α and JNK phosphorylation, and upregulated XBP-1 mRNA and protein expression. Moreover, p-eIF2α and CHOP expressions were clearly elevated in the Cd groups. Interestingly, PBA almost completely inhibited ER stress and protected spermatogonia against apoptosis induced by Cd. PBA alleviated Cd-induced ER stress and spermatogonia apoptosis, and may have the therapeutic role in Cd-induced male reproductive toxicity. • CdCl 2 induced spermatogonia apoptosis in vitro. • CdCl 2 triggered spermatogonia ER stress. • 4-PBA alleviated CdCl 2 -induced spermatogonia apoptosis. [ABSTRACT FROM AUTHOR]
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- 2024
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3. 1-methylcyclopropene combined with ethylene absorbent delays the ripening of 'Fenjiao' banana (Musa ABB Pisang Awak).
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Wang, Rong, Zhang, Lan, Rahman, Faiz Ur, Luo, Jun, Liu, Tongxin, Chen, Weixin, Li, Xueping, and Zhu, Xiaoyang
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BANANAS , *PECTINESTERASE , *1-Methylcyclopropene , *PECTINS , *ETHYLENE , *PHYSIOLOGY , *NUTRITIONAL value , *GENE expression - Abstract
• 1-MCP + ethylene absorbent (EA) treatment increase shelf-life of 'Fenjiao' banana. • EA does not have the negative effect on the ripening of 'Fenjiao' banana. • 1-MCP+EA repress the enzymes activity related to fruit softening. • 1-MCP +EA modulate the expression of gene related of ripening. • 1-MCP +EA treatment is easy to promote and apply in the banana industry. The 'Fenjiao' banana (Musa ABB Pisang Awak) has a high commercial and nutritional value and is harvested when it is highly plump at between 85 and 90 % commercial maturity. The fruit are less angular at this stage. However, these fruit soften rapidly after harvest. 1-Methylcyclopropene (1-MCP) significantly delays ripening, but it can cause ripening disorders when used improperly. Ethylene absorbent (EA) is also widely used to increase the postharvest life of fruit, but it has less of an effect on 'Fenjiao' banana. This study was conducted to optimize the concentrations of 1-MCP combined with EA to increase the shelf life of these bananas. The results showed that a low concentration of 1-MCP (7 g L−1) combined with EA (2 g kg−1) significantly prolonged the shelf life of the 'Fenjiao' banana and maintained its high quality. The combination of 1-MCP and EA repressed the activities of 1-aminocyclopropane-1-carboxylic acid (ACC) oxidase, ACC synthase, pectin methylesterase, polygalacturonase and pectate lyase in the peel and pulp of 'Fenjiao' banana, as well as the corresponding levels of expression of MbACS1, MbACO1, MbPG1, MbPL1 , except for MbPME1 , which are induced by 1-MCP. This study provides a useful technique for preserving 'Fenjiao' fruit with a study on its possible physiological mechanism, which could be applied in the postharvest production of 'Fenjiao' banana. [ABSTRACT FROM AUTHOR]
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- 2024
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4. PseUpred-ELPSO Is an Ensemble Learning Predictor with Particle Swarm Optimizer for Improving the Prediction of RNA Pseudouridine Sites.
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Wang, Xiao, Li, Pengfei, Wang, Rong, and Gao, Xu
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PSEUDOURIDINE , *RNA modification & restriction , *GENE expression , *RNA , *NON-coding RNA , *URIDINE - Abstract
Simple Summary: RNA pseudouridine modifications are present in various RNAs across different organisms and play crucial roles in regulating gene expression during biological processes. The accurate identification of pseudouridine sites within RNA sequences is essential for understanding their functional mechanisms. This study proposes a novel ensemble learning predictor named PseUpred-ELPSO, which accurately predicts RNA pseudouridine sites. The predictor demonstrates excellent performance in both cross-validation and independent testing. A user-friendly web server has been established, making it a powerful tool for pseudouridine site identification. RNA pseudouridine modification exists in different RNA types of many species, and it has a significant role in regulating the expression of biological processes. To understand the functional mechanisms for RNA pseudouridine sites, the accurate identification of pseudouridine sites in RNA sequences is essential. Although several fast and inexpensive computational methods have been proposed, the challenge of improving recognition accuracy and generalization still exists. This study proposed a novel ensemble predictor called PseUpred-ELPSO for improved RNA pseudouridine site prediction. After analyzing the nucleotide composition preferences between RNA pseudouridine site sequences, two feature representations were determined and fed into the stacking ensemble framework. Then, using five tree-based machine learning classifiers as base classifiers, 30-dimensional RNA profiles are constructed to represent RNA sequences, and using the PSO algorithm, the weights of the RNA profiles were searched to further enhance the representation. A logistic regression classifier was used as a meta-classifier to complete the final predictions. Compared to the most advanced predictors, the performance of PseUpred-ELPSO is superior in both cross-validation and the independent test. Based on the PseUpred-ELPSO predictor, a free and easy-to-operate web server has been established, which will be a powerful tool for pseudouridine site identification. [ABSTRACT FROM AUTHOR]
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- 2024
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5. Pharmacokinetic changes of norfloxacin based on expression of MRP2 after acute exposure to high altitude at 4300 m.
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Luo, Bingfeng, Wang, Rong, Li, Wenbin, Yang, Tao, Wang, Chang, Lu, Hui, Zhao, Anpeng, Zhang, Juanhong, and Jia, Zhengping
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PHARMACOKINETICS , *NORFLOXACIN , *GENE expression , *PHYSIOLOGICAL effects of altitudes , *LABORATORY rats - Abstract
Background This study was to investigate the influence of physiological changes and the expression of MRP2 efflux transporter on the pharmacokinetics of norfloxacin after acute exposure to high altitude 4300 m. Methods and Results The rats were randomly divided into high altitude group and plain group. Blood gas and biochemical analysis showed that the physiological parameters significantly changed at high altitude. The mRNA and protein expression of MRP2 in high altitude group were higher than plain group in rat small intestine and kidney, while was reduced in rat liver. The AUC, K a and C max of norfloxacin were significantly reduced in high altitude group (p < 0.05). However, the MRT, CL, t 1/2 and Vd were significantly increased (p < 0.05). Conclusions These results indicate that physiological indicators and expression levels of drug transporters MRP2 are changed in responded to high altitude, to severely affect norfloxacin pharmacokinetics. These changes may provide basis and new ideas to adjust the dosage and administration, so as to promote rational drug use in the high altitude. [ABSTRACT FROM AUTHOR]
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- 2017
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6. Ecdysteroid titers and expression of Halloween genes and ecdysteroid receptor in relation to overwintering and the long larval phase in the seabuckthorn carpenterworm, Holcocerus hippophaecolus.
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Wang, Rong, Zong, Shixiang, Luo, Youqing, Zhou, Jiao, Li, Juan, Weng, Qiang, and Sheng, Xia
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ECDYSONE , *TITERS , *GENE expression , *PRIONOXYSTUS robiniae , *LARVAE , *ANIMAL wintering - Abstract
The cytochrome P450 enzymes encoded by the Halloween genes - spook ( spo), phantom ( phm), disembodied ( dib), shadow ( sad), and shade ( shd) - catalyze a series of hydroxylation steps resulting in the active molting hormone 20-hydroxyecdysone (20E). This study investigated 20E and ecdysone titers and the expression profile of Halloween genes and ecdysone receptor ( EcR) during larval, pupal, and adult stages in seabuckthorn carpenterworm, Holcocerus hippophaecolus Hua ( Lepidoptera: Cossidae). Hh-spo, Hh-phm, Hh-dib, and Hh-sad showed predominant expression in the prothoracic gland at the larval stage, whereas Hh-shd and Hh-EcR were significantly expressed in the fat body. The mRNA levels of Hh-spo, Hh-phm, Hh-dib, Hh-shd, Hh-sad, and Hh-EcR were lowest from late October to middle April, when the insects were in overwintering dormancy, but began to increase from May each year, when the insects were terminating quiescence. Concomitant with the changes in these genes, 20E and ecdysone titers gradually increased during the 4-year life cycle of H. hippophaecolus. These data indicate that the seasonal expressions of Hh-spo, Hh-phm, Hh-shd, and Hh-EcR play crucial roles in quiescence of the overwintering period, and are responsible for the long larval phase and the exact timing and amplitude of the ecdysteroid titer required for the coordination of growth and development in H. hippophaecolus. [ABSTRACT FROM AUTHOR]
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- 2016
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7. Unique MicroRNA signatures associated with early coronary atherosclerotic plaques.
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Wang, Rong, Dong, Lai-Dong, Meng, Xiang-Bin, Shi, Qing, and Sun, Wen-Yu
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MICRORNA , *ATHEROSCLEROTIC plaque , *PATHOLOGICAL physiology , *EARLY diagnosis , *CARDIOVASCULAR diseases , *GENE expression - Abstract
The pathophysiology of coronary atherosclerotic plaques is a complex process. Early detection of coronary atherosclerotic plaques is critical in the prevention, prognostic and therapeutic intervention of cardiovascular disease. MicroRNAs (miRNAs), endogenous short non-coding RNAs, have been reported to play an important role in cardiovascular diseases and are also used as disease markers. However, the miRNA expression profile in early coronary atherosclerotic plaques has yet been reported. We hypothesize that miRNAs can be used as effective disease markers for detection of early coronary atherosclerotic plaques. In this analysis, coronary artery samples from three patients with early coronary atherosclerosis were harvested and miRNA expression profile determined using microarray analysis. Compared with healthy controls, a total of 44 miRNAs were upregulated and 57 miRNAs were downregulated. Among the dysregulated miRNAs, eight were significantly upregulated while five miRNAs were significantly downregulated, as determined by t- test ( P < 0.05). Four of the significantly dysregulated miRNAs, including miR-221, miR-155, miR-100 and hsa-miR-1273, were selected and verified by real-time PCR. The real-time PCR results were consistent with the microarray data that miR-221, miR-155 and miR-100 were significantly downregulated in plaques, whereas miR-1273 was significantly upregulated. These results indicate that miRNAs expression level can be used as potential markers for early coronary atherosclerotic plaque formation. [ABSTRACT FROM AUTHOR]
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- 2015
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8. Retinoic Acid Receptor-β Gene Reexpression and Biological Activity in SHI-1 Cells after Combined Treatment with 5-Aza-2′-Deoxycytidine and All-Trans Retinoic Acid.
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Xiang, Lili, Wang, Rong, Wei, Jiang, Qiu, Guoqiang, Cen, Jiannong, Hu, Shaoyan, Xie, Xiaobao, Chen, Zixing, and Gu, Weiying
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RETINOIC acid receptors , *GENE expression , *ACUTE myeloid leukemia treatment , *COMBINATION drug therapy , *DEOXYCYTIDINE , *APOPTOSIS inhibition , *DNA methylation , *THERAPEUTICS - Abstract
Background: This study was conducted to determine the antineoplastic activities of 5-aza-2′-deoxycytidine (decitabine; DAC) and all-trans retinoic acid (ATRA), administered either alone or in combination, on in vitro cultured SHI-1 cells as well as their effects on the expression of the tumor suppressor gene p16INK4a (p16) and the retinoic acid receptor (RAR)-β. Methods: Cellgrowth inhibition, differentiation and apoptosis were determined in SHI-1 cells treated with DAC and/or ATRA, and the combination index of the two compounds was calculated. Methylation of the p16 and RAR-β genes in SHI-1 cells was detected by methylation-specific polymerase chain reaction (PCR). Real-time quantitative reverse transcriptase PCR was used to detect mRNA expression of the p16 and RAR-β genes, and Western blot analysis was performed for protein expression. Results: The drug combination had a synergistic effect on growth inhibition, differentiation and apoptosis of SHI-1 cells, and the effects of DAC and ATRA weredependent on time. DAC, either alone or in combination with ATRA, induced demethylation of the genes p16 and RAR-β, whereas ATRA alone had no effect on methylation. The RAR-β gene was reexpressed following DAC-ATRA combination treatment, and both agents had no effect on p16 expression. Conclusion: The results revealed that DAC used in combination with ATRA has significant clinical potential in the treatment of acute monocytic leukemia. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]
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- 2015
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9. Perk Gene Dosage Regulates Glucose Homeostasis by Modulating Pancreatic β-Cell Functions.
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Wang, Rong, Munoz, Elyse E., Zhu, Siying, McGrath, Barbara C., and Cavener, Douglas R.
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TRANSLATION initiation factors (Biochemistry) , *GLUCOSE metabolism , *PANCREATIC beta cells , *HOMEOSTASIS , *INSULIN synthesis , *CELL proliferation , *GENETIC regulation , *CELL physiology , *DIABETES - Abstract
Background: Insulin synthesis and cell proliferation are under tight regulation in pancreatic β-cells to maintain glucose homeostasis. Dysfunction in either aspect leads to development of diabetes. PERK (EIF2AK3) loss of function mutations in humans and mice exhibit permanent neonatal diabetes that is characterized by insufficient β-cell mass and reduced proinsulin trafficking and insulin secretion. Unexpectedly, we found that Perk heterozygous mice displayed lower blood glucose levels. Methodology: Longitudinal studies were conducted to assess serum glucose and insulin, intracellular insulin synthesis and storage, insulin secretion, and β-cell proliferation in Perk heterozygous mice. In addition, modulation of Perk dosage specifically in β-cells showed that the glucose homeostasis phenotype of Perk heterozygous mice is determined by reduced expression of PERK in the β-cells. Principal Findings: We found that Perk heterozygous mice first exhibited enhanced insulin synthesis and secretion during neonatal and juvenile development followed by enhanced β-cell proliferation and a substantial increase in β-cell mass at the adult stage. These differences are not likely to entail the well-known function of PERK to regulate the ER stress response in cultured cells as several markers for ER stress were not differentially expressed in Perk heterozygous mice. Conclusions: In addition to the essential functions of PERK in β-cells as revealed by severely diabetic phenotype in humans and mice completely deficient for PERK, reducing Perk gene expression by half showed that intermediate levels of PERK have a profound impact on β-cell functions and glucose homeostasis. These results suggest that an optimal level of PERK expression is necessary to balance several parameters of β-cell function and growth in order to achieve normoglycemia. [ABSTRACT FROM AUTHOR]
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- 2014
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10. Enhancing neutralizing antibody production by an interferon-inducing porcine reproductive and respiratory syndrome virus strain.
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Wang, Rong, Xiao, Yueqiang, Opriessnig, Tanja, Ding, Yi, Yu, Ying, Nan, Yuchen, Ma, Zexu, Halbur, Patrick G., and Zhang, Yan-Jin
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IMMUNOGLOBULINS , *INTERFERONS , *PORCINE reproductive & respiratory syndrome , *GENE expression , *ACETYLIDES , *LUNG diseases - Abstract
Highlights: [•] The interferon-inducing PRRSV strain A2MC2 elicited higher neutralizing antibodies. [•] A2MC2 induced earlier onset and higher levels of the antibodies than the MLV. [•] The A2MC2-induced antibodies were able to neutralize heterologous VR-2385. [•] A2MC2 induced higher expression of IFN-γ in PAMs than the MLV. [ABSTRACT FROM AUTHOR]
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- 2013
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11. Induction of STAT1 Phosphorylation at Serine 727 and Expression of Proinflammatory Cytokines by Porcine Reproductive and Respiratory Syndrome Virus.
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Yu, Ying, Wang, Rong, Nan, Yuchen, Zhang, Linsheng, and Zhang, Yanjin
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PHOSPHORYLATION , *GENE expression , *CYTOKINES , *PORCINE reproductive & respiratory syndrome , *ETIOLOGY of diseases , *IMMUNE system , *VETERINARY medicine , *LABORATORY swine - Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is a viral pathogen that causes acute respiratory illnesses in young pigs. Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis. [ABSTRACT FROM AUTHOR]
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- 2013
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12. Differential expression of genes and changes in glucose metabolism in the liver of liver-specific glucokinase gene knockout mice
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Wang, Rong, Gao, Hui, Xu, Wei, Li, Hui, Mao, Yiqing, Wang, Yi, Guo, Tingting, Wang, Xi, Song, Rongjing, Li, Zhixin, Irwin, David M., Niu, Gang, and Tan, Huanran
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GENE expression , *GLUCOSE metabolism , *GLUCOKINASE , *KNOCKOUT mice , *PEOPLE with diabetes , *GLYCOGEN phosphorylase , *GLYCOGEN synthases - Abstract
Abstract: To investigate the role of liver-specific expression of glucokinase (GCK) in the pathogenesis of hyperglycemia and to identify candidate genes involved in mechanisms of the onset and progression of maturity onset diabetes of the young, type 2 (MODY-2), we examined changes in biochemical parameters and gene expression in GCK knockout (gckw/–) and wild-type (gckw/w) mice as they aged. Fasting blood glucose levels were found to be significantly higher in the gckw/– mice, compared to age-matched gckw/w mice, at all ages (P <0.05), except at 2weeks. GCK activity of gckw/– mice was about 50% of that of wild type (gckw/w) mice (P <0.05). Glycogen content at 4 and 40weeks of age was lower in gckw/– mice compared to gckw/w mice. Differentially expressed genes in the livers of 2 and 26week-old liver-specific GCK knockout (gckw/–) mice were identified by suppression subtractive hybridization (SSH), which resulted in the identification of phosphoenolpyruvatecarboxykinase (PEPCK, also called PCK1) and Sterol O-acyltransferase 2 (SOAT2) as candidate genes involved in pathogenesis. The expressions of PEPCK and SOAT2 along with glycogen phosphorylase (GP) and glycogen synthase (GS) were then examined in GCK knockout (gckw/–) and wild-type (gckw/w) mice at different ages. Changes in PEPCK mRNA levels were confirmed by real-time RT-PCR, while no differences in the levels of expression of SOAT2 or GS were observed in age-matched GCK knockout (gckw/–) and wild-type (gckw/w) mice. GP mRNA levels were decreased in 40-week old gckw/– mice compared to age-matched gckw/w mice. Changes in gluconeogenesis, delayed development of GCK and impaired hepatic glycogen synthesis in the liver potentially lead to the onset and progression of MODY2. [Copyright &y& Elsevier]
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- 2013
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13. GP120-specific exosome-targeted T cell-based vaccine capable of stimulating DC- and CD4+ T-independent CTL responses
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Nanjundappa, Roopa Hebbandi, Wang, Rong, Xie, Yufeng, Umeshappa, Channakeshava Sokke, Chibbar, Rajni, Wei, Yangdou, Liu, Qiang, and Xiang, Jim
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HIGHLY active antiretroviral therapy , *T cells , *IMMUNIZATION , *GLYCOPROTEINS , *CD antigens , *DENDRITIC cells , *GENE expression , *IMMUNITY - Abstract
Abstract: The limitations of highly active anti-retroviral therapy (HAART) have necessitated the development of alternative therapeutics. In this study, we generated ovalbumin (OVA)-pulsed and pcDNAgp120-transfected dendritic cell (DC)-released exosomes (EXOova and EXOgp120) and ConA-stimulated C57BL/6 CD8+ T cells. OVA- and Gp120-Texo vaccines were generated from CD8+ T cells with uptake of EXOova and EXOgp120, respectively. We demonstrate that OVA-Texo stimulates in vitro and in vivo OVA-specific CD4+ and CD8+ cytotoxic T lymphocyte (CTL) responses leading to long-term immunity against OVA-expressing BL6-10OVA melanoma. Interestingly, CD8+ T cell responses are DC and CD4+ T cell independent. Importantly, Gp120-Texo also stimulates Gp120-specific CTL responses and long-term immunity against Gp120-expressing B16 melanoma. Therefore, this novel HIV-1-specific EXO-targeted Gp120-Texo vaccine may be useful in induction of efficient CTL responses in AIDS patients with DC dysfunction and CD4+ T cell deficiency. [Copyright &y& Elsevier]
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- 2011
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14. Gene expression profiling of the androgen receptor antagonists flutamide and vinclozolin in zebrafish (Danio rerio) gonads
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Martinović-Weigelt, Dalma, Wang, Rong-Lin, Villeneuve, Daniel L., Bencic, David C., Lazorchak, Jim, and Ankley, Gerald T.
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GENE expression , *ANTIANDROGENS , *FLUTAMIDE , *VINCLOZOLIN , *ZEBRA danio , *GONADS , *ENDOCRINE disruptors , *BIOMARKERS , *DNA microarrays - Abstract
Abstract: The studies presented in this manuscript focus on characterization of transcriptomic responses to anti-androgens in zebrafish (Danio rerio). Research on the effects of anti-androgens in fish has been characterized by a heavy reliance on apical endpoints, and molecular mechanisms of action (MOA) of anti-androgens remain poorly elucidated. In the present study, we examined effects of a short term exposure (24–96h) to the androgen receptor antagonists flutamide (FLU) and vinclozolin (VZ) on gene expression in gonads of sexually mature zebrafish, using commercially available zebrafish oligonucleotide microarrays (4×44K platform). We found that VZ and FLU potentially impact reproductive processes via multiple pathways related to steroidogenesis, spermatogenesis, and fertilization. Observed changes in gene expression often were shared by VZ and FLU, as demonstrated by overlap in differentially-expressed genes and enrichment of several common key pathways including: (1) integrin and actin signaling, (2) nuclear receptor 5A1 signaling, (3) fibroblast growth factor receptor signaling, (4) polyamine synthesis, and (5) androgen synthesis. This information should prove useful to elucidating specific mechanisms of reproductive effects of anti-androgens in fish, as well as developing biomarkers for this important class of endocrine-active chemicals. [ABSTRACT FROM AUTHOR]
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- 2011
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15. Expression of Neuropilin-2 in salivary adenoid cystic carcinoma: Its implication in tumor progression and angiogenesis
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Cai, Yu, Wang, Rong, Zhao, Yi-Fang, Jia, Jun, Sun, Zhi-Jun, and Chen, Xin-Ming
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NEUROPILINS , *GENE expression , *SALIVARY gland cancer , *CANCER invasiveness , *CELL membranes , *CANCER cells - Abstract
Abstract: Neuropilin-2(Nrp2), which is a nontyrosine kinase transmembrane glycoprotein, can promote angiogenesis and is a poor prognostic factor in some human cancers. In the present study, to explore the expression and potential function of Nrp2 in salivary adenoid cystic carcinoma (SACC), immunohistochemistry was used to examine the Nrp2 expression in 50 SACCs and 20 normal salivary gland tissues nearby SACCs. The result showed that immunoreactivity for Nrp2 was detected in 47 of 50 SACCs, and its expression level had significant correlations with microvessel density, tumor size, TMN clinical stage, vascular invasion, and metastasis (P <0.05) of SACCs. In addition, inhibition of Nrp2 function by the receptor–ligand interaction-blocking antibody decreased cell migration, invasion, and angiogenic promotion without influences on the cell proliferation of Acc-3 cells. Taken together, the expression of Nrp2 protein is significantly correlated with tumor progression and angiogenesis in SACCs. These results suggest that Nrp2 may be a potential therapeutic target for SACCs. [ABSTRACT FROM AUTHOR]
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- 2010
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16. Simvastatin inhibits acidic extracellular pH-activated, outward rectifying chloride currents in RAW264.7 monocytic-macrophage and human peripheral monocytes
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Shi, Cheng-yao, Wang, Rong, Liu, Chun-xi, Jiang, Hao, Ma, Zhi-yong, Li, Li, and Zhang, Wei
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STATINS (Cardiovascular agents) , *IMMUNOSUPPRESSION , *GENE expression , *ACIDOSIS , *CHLORIDES in the body , *MACROPHAGES , *MONOCYTES , *HYDROGEN-ion concentration - Abstract
Abstract: Extracellular acidic pH activated chloride channels (ICl,acid) have been characterized in HEK 293 cells and mammalian cardiac myocytes. This study was designed to evaluate the expression of ICl,acid in RAW264.7 monocytic-macrophage and human peripheral monocytes and to investigate the effect of simvastatin on ICl,acid. In two kinds of cells, the activation and deactivation of the current rapidly and repeatedly followed the change of the extracellular solution to pH=4.3. Compared with the outward current (pA/pF) activated at pH 4.3, the currents inhibited by simvastatin at concentrations of 0.1 μM were all decreased a little, however the currents at concentrations of 1 μM and 10 μM simvastatin were decreased significantly. The IC50 for simvastatin inhibiting ICl,acid of RAW264.7 was 13.77 μM. In summary, we report for the first time that simvastatin inhibits the ICl,acid of RAW264.7 monocytic-macrophage and human peripheral monocytes in a concentration-dependent manner. [Copyright &y& Elsevier]
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- 2009
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17. PSAT1 enhances the efficacy of the prognosis estimation nomogram model in stage-based clear cell renal cell carcinoma.
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Wang, Jun, He, Xiaoming, Mi, Yuanyuan, Chen, Yong Q., Li, Jie, and Wang, Rong
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RENAL cell carcinoma , *PROGNOSTIC models , *NOMOGRAPHY (Mathematics) , *GENE expression , *OVERALL survival - Abstract
Background: Clear cell renal cell carcinoma (ccRCC) is associated with a high prevalence of cancer-related deaths. The survival rates of patients are significantly lower in late-stage ccRCC than in early-stage ccRCC, due to the spread and metastasis of late-stage ccRCC, surgery has not reached the goal of radical cure, and the effect of traditional radiotherapy and chemotherapy is poor. Thus, it is crucial to accurately assess the prognosis and provide personalized treatment at an early stage in ccRCC. This study aims to develop an efficient nomogram model for stratifying and predicting the survival of ccRCC patients based on tumor stage. Methods: We first analyzed the microarray expression data of ccRCC patients from the Gene Expression Omnibus (GEO) database and categorized them into two groups based on the disease stage (early and late stage). Subsequently, the GEO2R tool was applied to screen out the genes that were highly expressed in all GEO datasets. Finally, the clinicopathological data of the two patient groups were obtained from The Cancer Genome Atlas (TCGA) database, and the differences were compared between groups. Survival analysis was performed to evaluate the prognostic value of candidate genes (PSAT1, PRAME, and KDELR3) in ccRCC patients. Based on the screened gene PSAT1 and clinical parameters that were significantly associated with patient prognosis, we established a new nomogram model, which was further optimized to a single clinical variable-based model. The expression level of PSAT1 in ccRCC tissues was further verified by qRT-PCR, Western blotting, and immunohistochemical analysis. Results: The datasets GSE73731, GSE89563, and GSE150404 identified a total of 22, 89, and 120 over-expressed differentially expressed genes (DEGs), respectively. Among these profiles, there were three genes that appeared in all three datasets based on different stage groups. The overall survival (OS) of late-stage patients was significantly shorter than that of early-stage patients. Among the three candidate genes (PSAT1, PRAME, and KDELR3), PSAT1 was shown to be associated with the OS of patients with late-stage ccRCC. Multivariate Cox regression analysis showed that age, tumor grade, neoadjuvant therapy, and PSAT1 level were significantly associated with patient prognosis. The concordance indices were 0.758 and 0.725 for the 3-year and 5-year OS, respectively. The new model demonstrated superior discrimination and calibration compared with the single clinical variable model. The enhancer PSAT1 used in the new model was shown to be significantly overexpressed in tissues from patients with late-stage ccRCC, as demonstrated by the mRNA level, protein level, and pathological evaluation. Conclusion: The new prognostic prediction nomogram model of PSAT1 and clinicopathological variables combined was thus established, which may provide a new direction for individualized treatment for different-stage ccRCC patients. [ABSTRACT FROM AUTHOR]
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- 2024
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18. Melatonin and Expression of Tryptophan Decarboxylase Gene (TDC) in Herbaceous Peony (Paeonia lactiflora Pall.) Flowers.
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Zhao, Daqiu, Wang, Rong, Liu, Ding, Wu, Yanqing, Sun, Jing, and Tao, Jun
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MELATONIN , *TRYPTOPHAN , *ANTIOXIDANTS , *PINEAL gland secretions , *HORMONES - Abstract
Melatonin is a bioactive, edible ingredient that promotes human health and exists widely in plants, but little is known about its biosynthetic routes and underlying molecular mechanisms in the herbaceous peony. In this contribution, we found that herbaceous peony flowers are rich in melatonin that is found in the greatest quantities in the white series, followed by the ink series, the red series and then the pink series. On this basis, the melatonin content fluctuates during flower development and peaks during the bloom stage. Moreover, it is apparent that sun exposure and blue light induce melatonin production whereas green light restrains it during a 24-h light/dark cycle of melatonin content, as there were ‘dual peaks’ at 2 p.m. and 2 a.m. Additionally, the corresponding expression pattern of the herbaceous peony tryptophan decarboxylase gene (
TDC ) was positively related with melatonin production. These results suggest that color series, development stage and light play an important role in melatonin accumulation, and thatTDC is a rate-limiting gene in melatonin biosynthesis. [ABSTRACT FROM AUTHOR]- Published
- 2018
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19. miRNA-381-3p Functions as a Tumor Suppressor to Inhibit Gastric Cancer by Targeting Fibroblast Growth Factor Receptor-2.
- Author
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Gao, Xiang, Liu, Huiqi, Wu, Qiong, Wang, Rong, Huang, Mingyu, Ma, Qiang, and Liu, Yongnian
- Subjects
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STOMACH tumors , *FIBROBLAST growth factors , *FLOW cytometry , *CANCER invasiveness , *MICRORNA , *CELL receptors , *APOPTOSIS , *METASTASIS , *GENE expression , *CELL motility , *TUMOR suppressor genes , *TISSUES , *RESEARCH funding , *CELL proliferation , *CELL lines , *POLYMERASE chain reaction - Abstract
Objectives: MicroRNAs possess essential effects on gastric cancer (GC), whereas the underlying mechanisms have not been fully uncovered. The present work focused on investigating the role of miR-381-3p in GC cellular processes and the possible mechanisms. Materials and Methods: miR-381-3p levels within GC tissues and cells were measured through quantitative real-time polymerase chain reaction (qRT-PCR). This study measured cell proliferation, apoptosis, and metastasis through EdU, colony formation, flow cytometry, and Transwell assays separately. TargetScan was adopted to predict the miR-381-3p targets, whereas luciferase reporter assay was adopted for confirmation. Results: miR-381-3p levels were decreased, whereas fibroblast growth factor receptor-2 (FGFR2) expression was increased in GC. miR-381-3p upregulation inhibited proliferation, migration, and invasion and it promoted the apoptosis of GC cells. Further, FGFR2 overexpression partly reversed the miR-381-3p-mediated impacts on GC cellular processes. Conclusions: This study provides an experimental basis, suggesting the potential of using miR-381-3p as the novel marker for GC. Clinical Trial Registration number: 2020-05. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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20. Neuroprotective Effects of Cerebral Ischemic Preconditioning in a Rat Middle Cerebral Artery Occlusion Model: The Role of the Notch Signaling Pathway.
- Author
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Chen, Li, Huang, Kuan, Wang, Rong, Jiang, Qiong, Wu, Zhenghua, Liang, Weidong, Guo, Rui, and Wang, Lifeng
- Subjects
- *
ANIMAL experimentation , *APOPTOSIS , *CALCIUM-binding proteins , *CELL receptors , *CELLULAR signal transduction , *CEREBRAL arteries , *GENE expression , *RATS , *REPERFUSION , *STEM cells , *TREATMENT effectiveness , *IN vitro studies , *IN vivo studies , *ISCHEMIC preconditioning ,CEREBRAL ischemia treatment - Abstract
Cerebral ischemia-reperfusion (I/R) injury is a major problem worldwide. The Notch signaling pathway plays an important role in neural progenitor cell differentiation and in the inflammatory response after central nervous system injury. This study evaluated whether the neuroprotective effect of cerebral ischemic preconditioning (cIPC) is mediated by the preactivation of the Notch signaling pathway. A rat middle cerebral artery occlusion/reperfusion (MCAO/R) model and glucose deprivation/reoxygenation (OGD/R) cell model were constructed to detect the neuroprotective effects of cIPC. In in vivo experiments, cIPC reduces the neurological functional deficit, cerebral infarction, and cellular apoptosis in the hippocampus induced by middle cerebral artery occlusion/reperfusion (MCAO/R), thus indicating that cIPC can improve neurologic function. Moreover, cIPC can reveal the expression peak of Jagged1, Notch1, NICD, and Hes1 protein, thereby indicating that cIPC can preactivate Notch signaling. However, cIPC-induced improvements in neurologic function are compromised by the γ-secretase inhibitor N-(N-(3,5-difluorophenacetyl)-1-alanyl)-S-phenylglycine t-butyl ester (DAPT). In in vitro experiments, OGD preconditioning (OGDPC) can clearly upregulate Notch1 expression in the OGD/R-treated neuron and neural stem cell. Notch1 pre-overexpression can decrease neuron death and apoptosis under OGD/R treatment. Notch1 pre-overexpression can decrease the percentage of G1 stage cells and increase the percentage of S stage cells in OGD/R-treated neural stem cell. Furthermore, Notch1 pre-knockdown has the opposite effect on cell survival, apoptosis, and cycle in both OGD/R-treated neuron and neural stem cell. In conclusion, our results demonstrate that the neuroprotective effects of cIPC in a rat MCAO/R model are mediated by the preactivation of the Notch signaling pathway. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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21. Genes associated with inflammation and the cell cycle may serve as biomarkers for the diagnosis and prognosis of acute myocardial infarction in a Chinese population.
- Author
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Su, Jiang, Gao, Changqing, Wang, Rong, Xiao, Cangsong, and Yang, Ming
- Subjects
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CELL cycle , *MYOCARDIAL infarction , *PUBLIC health , *GENE expression , *MICRORNA , *STAT proteins - Abstract
The present study aimed to identify biomarkers for the clinical diagnosis of acute myocardial infarction (AMI) in a Chinese population using microarray data collected from the Gene Expression Omnibus database under accession number GSE97320. This included the peripheral blood samples of three patients with AMI and three controls. Differentially expressed genes (DEGs) were identified using the limma package and protein‑protein interaction networks were constructed using data from the Search Tool for the Retrieval of Interacting Genes database, followed by module analysis to screen for hub genes. Functional enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery. The identified genes were verified by overlapping with the target genes of microRNAs (miRs) known to be associated with AMI, as well as the DEGs identified in other AMI datasets, including GSE24519, GSE34198 and GSE48060. As a result, 752 DEGs (449 upregulated and 303 downregulated) were identified in the GSE97320 dataset. The upregulated DEGs were predicted to participate in inflammatory pathways, including the toll‑like receptor (TLR) signaling pathway, including ras‑related C3 botulinum toxin substrate 1 (RAC1), TLR4, C‑C motif chemokine receptor (CCR)1; cytokine‑cytokine receptor interaction, including signal transducer and activator of transcription (STAT)3; chemokine signaling pathway, including CCR10; pathways associated with cancer, including colony stimulating factor 3 receptor (CSF3R); and leukocyte transendothelial migration, including matrix metallopeptidase 9 (MMP9). The downregulated DEGs were associated with the cell cycle, including alstrom syndrome protein 1 (ALMS1). These conclusions were made following functional analysis of the genes in the three identified modules. MMP9, TLR4, STAT3, CCR1 and ALMS1 were regulated by miR‑21‑5p, whereas RAC1 was regulated by miR‑30c‑5p. A comparison among the four datasets confirmed the roles of CSF3R and CCR10. HtrA serine peptidase 1 (HTRA1) was the only gene associated with both mortality and recurrence. In conclusion, inflammation‑associated genes, including STAT3, CCR1, RAC1, MMP9, CCR10, CSF3R and HTRA1, as well as cell cycle‑associated genes such as ALMS1, may be biomarkers for the diagnosis and prognosis of AMI in Chinese people. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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22. Cross talk of chromosome instability, CpG island methylator phenotype and mismatch repair in colorectal cancer.
- Author
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Zhang, Tian-Ming, Huang, Tao, and Wang, Rong-Fei
- Subjects
- *
CHROMOSOMES , *COLON cancer patients , *GENE expression , *PHENOTYPES , *RANDOM walks - Abstract
Colorectal cancer is a severe cancer associated with a high prevalence and fatality rate. There are three major mechanisms for colorectal cancer: (1) Chromosome instability (CIN), (2) CpG island methylator phenotype (CIMP) and (3) mismatch repair (MMR), of which CIN is the most common type. However, these subtypes are not exclusive and overlap. To investigate their biological mechanisms and cross talk, the gene expression profiles of 585 colorectal cancer patients with CIN, CIMP and MMR status records were collected. By comparing the CIN+ and CIN- samples, CIMP+ and CIMP- samples, MMR+ and MMR- samples with minimal redundancy maximal relevance (mRMR) and incremental feature selection (IFS) methods, the CIN, CIMP and MMR associated genes were selected. Unfortunately, there was little direct overlap among them. To investigate their indirect interactions, downstream genes of CIN, CIMP and MMR were identified using the random walk with restart (RWR) method and a greater overlap of downstream genes was indicated. The common downstream genes were involved in biosynthetic and metabolic pathways. These findings were consistent with the clinical observation of wide range metabolite aberrations in colorectal cancer. To conclude, the present study gave a gene level explanation of CIN, CIMP and MMR, but also showed the network level cross talk of CIN, CIMP and MMR. The common genes of CIN, CIMP and MMR may be useful for cross-subtype general colorectal cancer drug development. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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23. Ion channel gene expression predicts survival in glioma patients.
- Author
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Wang, Rong, Gurguis, Christopher I., Gu, Wanjun, Ko, Eun A, Lim, Inja, Bang, Hyoweon, Zhou, Tong, and Ko, Jae-Hong
- Subjects
- *
GLIOMAS , *GENE expression , *ION channels , *CELL proliferation , *CELL migration , *PATIENTS - Abstract
Ion channels are important regulators in cell proliferation, migration, and apoptosis. The malfunction and/or aberrant expression of ion channels may disrupt these important biological processes and influence cancer progression. In this study, we investigate the expression pattern of ion channel genes in glioma. We designate 18 ion channel genes that are differentially expressed in high-grade glioma as a prognostic molecular signature. This ion channel gene expression based signature predicts glioma outcome in three independent validation cohorts. Interestingly, 16 of these 18 genes were down-regulated in high-grade glioma. This signature is independent of traditional clinical, molecular, and histological factors. Resampling tests indicate that the prognostic power of the signature outperforms random gene sets selected from human genome in all the validation cohorts. More importantly, this signature performs better than the random gene signatures selected from glioma-associated genes in two out of three validation datasets. This study implicates ion channels in brain cancer, thus expanding on knowledge of their roles in other cancers. Individualized profiling of ion channel gene expression serves as a superior and independent prognostic tool for glioma patients. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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24. Prediction and Validation of Hub Genes Associated with Colorectal Cancer by Integrating PPI Network and Gene Expression Data.
- Author
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Xiong, Yongfu, You, Wenxian, Wang, Rong, Peng, Linglong, and Fu, Zhongxue
- Subjects
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COLON tumors , *GENE expression , *GENOMICS , *GENETICS ,RECTUM tumors - Abstract
Although hundreds of colorectal cancer- (CRC-) related genes have been screened, the significant hub genes still need to be further identified. The aim of this study was to identify the hub genes based on protein-protein interaction network and uncover their clinical value. Firstly, 645 CRC patients’ data from the Tumor Cancer Genome Atlas were downloaded and analyzed to screen the differential expression genes (DEGs). And then, the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was performed, and PPI network of the DEGs was constructed by Cytoscape software. Finally, four hub genes (CXCL3, ELF5, TIMP1, and PHLPP2) were obtained from four subnets and further validated in our clinical setting and TCGA dataset. The results showed that mRNA expression of CXCL3, ELF5, and TIMP1 was increased in CRC tissues, whereas PHLPP2 mRNA expression was decreased. More importantly, high expression of CXCL3, ELF5, and TIMP1 was significantly associated with lymphatic invasion, distance metastasis, and advanced tumor stage. In addition, a shorter overall survival was observed in patients with increased CXCL3, TIMP1, and ELF5 expression and decreased PHLPP2 expression. In conclusion, the four hub genes screened by our strategy could serve as novel biomarkers for prognosis prediction of CRC patients. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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25. Lnc-HZ03 promotes TRBP-mediated splicing of pre-miR-hz03 to generate miR-hz03 in human trophoblast cells.
- Author
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Zhao, Jingsong, Cheng, Liqin, Liu, Qicai, Liang, Tingting, Xie, Jiayu, Wang, Rong, Chen, Weina, Ao, Lin, and Zhang, Huidong
- Subjects
- *
GENE expression , *RECURRENT miscarriage , *RNA-binding proteins , *RNA regulation , *MISCARRIAGE , *TROPHOBLAST - Abstract
Benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) leads to dysfunctions of human trophoblast cells and further induces miscarriage. In our previous study, we have found that lnc-HZ03 and miR-hz03 are upregulated in BPDE-exposed human trophoblast cells and in recurrent miscarriage tissues; and the upregulated miR-hz03 caused by lnc-HZ03 further promotes the apoptosis of human trophoblast cells and induces miscarriage. However, how lnc-HZ03 upregulates miR-hz03 is completely unknown. In this study, we find that lnc-HZ03 upregulates the expression level of a transcription factor TFIID (a TATA-binding protein) and promotes TFIID-mediated transactivation response element RNA-binding protein (TRBP) transcription. Subsequently, the upregulated TRBP promotes the maturation of miR-hz03 by splicing its precursor pre-miR-hz03 in human trophoblast cells. In BPDE-exposed trophoblast cells or in recurrent miscarriage tissues, lnc-HZ03 was upregulated, which accelerates the TFIID-mediated TRBP transcription and thus promotes TRBP-mediated miR-HZ03 maturation. Subsequently, the upregulated miR-hz03 further promotes the apoptosis of human trophoblast cells and induces miscarriage. This work provides new insights into the regulation of miRNA expression levels by lncRNAs in BPDE-exposed human trophoblast cells. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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- View/download PDF
26. Free docosahexaenoic acid promotes ferroptotic cell death via lipoxygenase dependent and independent pathways in cancer cells.
- Author
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Shan, Kai, Feng, Ninghan, Zhu, Doudou, Qu, Hongyan, Fu, Guoling, Li, Jiaqi, Cui, Jing, Chen, Heyan, Wang, Rong, Qi, Yumin, and Chen, Yong Q.
- Subjects
- *
DOCOSAHEXAENOIC acid , *FLOW cytometry , *HIGH performance liquid chromatography , *XENOGRAFTS , *AUTOPHAGY , *APOPTOSIS , *CELLULAR signal transduction , *GENE expression , *MASS spectrometry , *OXIDOREDUCTASES , *CELL lines , *BIOLOGICAL assay , *REACTIVE oxygen species , *CELL death , *FATTY acids - Abstract
Purpose: Ferroptosis is a form of regulated cell death that has the potential to be targeted as a cancer therapeutic strategy. But cancer cells have a wide range of sensitivities to ferroptosis, which limits its therapeutic potential. Accumulation of lipid peroxides determines the occurrence of ferroptosis. However, the type of lipid involved in peroxidation and the mechanism of lipid peroxide accumulation are less studied. Methods: The effects of fatty acids (10 μM) with different carbon chain length and unsaturation on ferroptosis were evaluated by MTT and LDH release assay in cell lines derived from prostate cancer (PC3, 22RV1, DU145 and LNCaP), colorectal cancer (HT-29), cervical cancer (HeLa) and liver cancer (HepG2). Inhibitors of apoptosis, necroptosis, autophagy and ferroptosis were used to determine the type of cell death. Then the regulation of reactive oxygen species (ROS) and lipid peroxidation by docosahexaenoic acid (DHA) was measured by HPLC–MS and flow cytometry. The avtive form of DHA was determined by siRNA mediated gene silencing. The role of lipoxygenases was checked by inhibitors and gene silencing. Finally, the effect of DHA on ferroptosis-mediated tumor killing was verified in xenografts. Results: The sensitivity of ferroptosis was positively correlated with the unsaturation of exogenously added fatty acid. DHA (22:6 n-3) sensitized cancer cells to ferroptosis-inducing reagents (FINs) at the highest level in vitro and in vivo. In this process, DHA increased ROS accumulation, lipid peroxidation and protein oxidation independent of its membrane receptor, GPR120. Inhibition of long chain fatty acid-CoA ligases and lysophosphatidylcholine acyltransferases didn't affect the role of DHA. DHA-involved ferroptosis can be induced in both arachidonate lipoxygenase 5 (ALOX5) negative and positive cells. Down regulation of ALOX5 inhibited ferroptosis, while overexpression of ALOX5 promoted ferroptosis. Conclusion: DHA can effectively promote ferroptosis-mediated tumor killing by increasing intracellular lipid peroxidation. Both ALOX5 dependent and independent pathways are involved in DHA-FIN induced ferroptosis. And during this process, free DHA plays an important role. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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27. Low expression of MYCN promotes cisplatin resistance by suppressing cisplatin-induced apoptosis in epithelial ovarian cancer.
- Author
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Yu, Rao, Zhang, Hao, Wang, Rong, and Xiao, Lin
- Subjects
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GENE expression , *CISPLATIN , *OVARIAN epithelial cancer , *OVARIAN cancer , *APOPTOSIS , *BAX protein , *BCL-2 proteins - Abstract
Epithelial ovarian cancer (EOC) is the most common cause of gynecological cancer-associated mortality. Cisplatin is one of the most effective chemotherapeutic drugs used in EOC; however, its use can lead to relapse due to cisplatin resistance. MYCN sensitizes neuroblastoma to undergo cisplatin-induced apoptosis. However, to the best of our knowledge, there have been no studies to date on the association between MYCN and cisplatin resistance in EOC. Therefore, the present study assessed this association. Datasets from The Cancer Genome Atlas database were used. The overall survival (OS) of patients receiving platin-based therapy was analyzed using Kaplan-Meier Plotter software. RNA sequencing data of 300 patients with EOC were downloaded from cBioportal. The co-expressed genes were subjected to 'Kyoto Encyclopedia of Genes and Genomes' analysis using DAVID software. For gene set enrichment analysis, the expression matrix was separated according to the median expression of MYCN, which was selected for hallmark gene set enrichment. Immunohistochemistry was used to assess MYCN expression in EOC tissue. Western blotting was used to evaluate MYCN, p53, Bax and Bcl-2 protein expression levels in EOC cells. Cell viability and apoptosis were assessed using Cell Counting Kit-8 and flow cytometry, respectively. The results demonstrated that MYCN upregulation was associated with increased cisplatin sensitivity and prolonged OS of patients with EOC and patients receiving platin-based therapy. Cisplatin downregulated MYCN expression in cisplatin-sensitive, but not resistant, EOC cells. The genes co-expressed with MYCN were primarily involved in pathways involved in 'chemotherapeutic resistance' and 'apoptosis'. MYCN enriched the apoptosis and p53 signaling pathways in hallmark gene sets. Cells in which MYCN was knocked down demonstrated significantly increased cisplatin resistance; however, MYCN overexpression in cisplatin-resistant cells restored cisplatin sensitivity. Collectively, the present study demonstrated that MYCN downregulation promoted cisplatin resistance by suppressing cisplatin-induced apoptosis in EOC. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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28. NCOA4-mediated ferritinophagy participates in cadmium-triggered ferroptosis in spermatogonia.
- Author
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Jia, Didi, Zhang, Mingming, Li, Mengyuan, Gong, Wenjing, Huang, Wei, Wang, Rong, Chen, Yihang, Yin, Qizi, Wu, Jie, Jin, Zhongxiu, Wang, Juan, Liu, Yehao, Liang, Chunmei, and Ji, Yanli
- Subjects
- *
IRON overload , *FERRITIN , *REACTIVE oxygen species , *IRON ions , *GENE expression , *PROTEIN expression - Abstract
Cadmium (Cd) is a common pollutant with reproductive toxicity. Our previous study revealed that Cd triggered spermatogonia ferroptosis. However, the underlying mechanisms remain unclear. Nuclear receptor coactivator 4 (NCOA4) mediates ferritinophagy and specific degradation of ferritin through lysosomes, resulting in the release of ferrous ions. Excessive autophagy can lead to ferroptosis. This study investigated the role of autophagy in Cd-triggered ferroptosis using GC-1 spermatogonial (spg) cells which exposed to CdCl 2 (5 μM, 10 μM, or 20 μM) for 24 without/with CQ. The cells which transfected with Ncoa4-siRNA were used to explore the role of NCOA4-mediated ferritinophagy in Cd-triggered ferroptosis. The results revealed that Cd caused mitochondrial swelling, rupture of cristae, and vacuolar-like changes. The Cd-treated cells exhibited more autophagosomes. Simultaneously, Cd increased intracellular iron, reactive oxygen species, and malondialdehyde concentrations while decreasing glutathione content and Superoxide Dismutase-2 activity. Moreover, Cd upregulated mRNA levels of ferritinophagy-associated genes (Ncoa4, Lc3b and Fth1), as well as enhanced protein expression of NCOA4, LC3B, and FTH1. While Cd decreased the mRNA and protein expression of p62/SQSTM1. These results showed that Cd caused ferritinophagy and ferroptosis. The use of chloroquine to inhibit autophagy ameliorated Cd-induced iron overload and ferroptosis. Moreover, Ncoa4 knockdown in spermatogonia significantly reduced intracellular iron concentration and alleviated Cd-triggered ferroptosis. In conclusion, our findings demonstrate that Cd activates the ferritinophagy pathway mediated by NCOA4, resulting in iron accumulation through ferritin degradation. This causes oxidative stress, ultimately initiating ferroptosis in spermatogonia. Our results may provide new perspectives and potential strategies for preventing and treating Cd-induced reproductive toxicity. [Display omitted] • Cd causes iron overload and triggers ferroptosis in spermatogonia. • Cd induces ferritinophagy in spermatogonia. • CQ antagonizes against Cd-caused iron overload in spermatogonia. • NCOA4-mediated ferritinophagy participates in Cd-triggered ferroptosis. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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- View/download PDF
29. MiR‐205‐5p promotes lung cancer progression and is valuable for the diagnosis of lung cancer.
- Author
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Zhao, Yu‐Long, Zhang, Jia‐Xiang, Yang, Juan‐Juan, Wei, Yu‐Bo, Peng, Jie‐Fei, Fu, Chang‐Jin, Huang, Min‐Hua, Wang, Rong, Wang, Ping‐Yu, Sun, Guang‐Bin, and Xie, Shu‐Yang
- Subjects
- *
DISEASE progression , *REVERSE transcriptase polymerase chain reaction , *FLOW cytometry , *CELL culture , *CANCER invasiveness , *LUNG tumors , *MICRORNA , *METASTASIS , *GENE expression , *IMMUNOBLOTTING , *CELL survival , *CELL proliferation , *GENES , *TUMOR markers , *POLYMERASE chain reaction , *RECEIVER operating characteristic curves - Abstract
Background: MicroRNAs (miRNAs) function as potential diagnostic biomarkers in various cancers. This study aimed to evaluate the roles of miR‐205‐5p in lung cancer progression and diagnosis. Materials and Methods: MiR‐205‐5p was detected by quantitative real‐time PCR. The effect of miR‐205‐5p on cell proliferation and metastasis was estimated by MTT and flow cytometry. The expression of TP53INP1 and related genes was analyzed by immunoblotting. The diagnostic value of miR‐205‐5p was analyzed using receiver operating characteristic (ROC) curve analysis, sensitivity, and specificity. Results: The miR‐205‐5p was increased in lung cancer tissues. MiR‐205‐5p mimics were promoted but its inhibitor suppressed cell proliferation and metastasis compared with control treatment in vitro and in vivo. By regulating the 3′ untranslated region, miR‐205‐5p could negatively regulate TP53INP1 expression, which further inhibited the expression of RB1 and P21, but increased that of cyclinD1. Moreover, the serum miR‐205‐5p levels of patients with lung cancer were significantly higher than those of normal controls, and they were correlated with patients' gender, drinking status, and clinical stage. The area under the ROC curve of serum miR‐205‐5p in the diagnosis of non‐small‐cell lung cancer was 0.8250, respectively. The finding supported its possession of high diagnostic efficiency for lung cancer. Conclusions: MiR‐205‐5p promoted lung cancer cell proliferation and metastasis by negatively regulating the novel target TP53INP1, which further affected the expression of P21, RB1, and cyclin D1. Serum miR‐205‐5p is a novel and valuable biomarker for lung cancer diagnosis. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
30. Fulvestrant increases gefitinib sensitivity in non-small cell lung cancer cells by upregulating let-7c expression.
- Author
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Shen, Hua, Liu, Jinyuan, Wang, Rong, Qian, Xu, Xu, Ruitong, Xu, Tongpeng, Li, Qi, Wang, Lin, Shi, Zhumei, Zheng, Jitai, Chen, Qiudan, and Shu, Yongqian
- Subjects
- *
ESTRADIOL , *GEFITINIB , *LUNG cancer treatment , *CANCER cells , *GENETIC regulation , *GENE expression , *EPIDERMAL growth factor receptors , *GENETIC mutation , *THERAPEUTICS - Abstract
Abstract: Patients with non-small cell lung cancer (NSCLC) who have activating epidermal growth factor receptor (EGFR) mutations benefit from treatment with EGFR-tyrosine kinase inhibitors (EGFR-TKIs), namely, gefitinib and erlotinib. However, these patients eventually develop resistance to EGFR-TKIs. About 50% of this acquired resistance may be the result of a secondary mutation in the EGFR gene, such as the one corresponding to T790M. In our previous study, we found that combined treatment with fulvestrant and gefitinib decreases the proliferation of H1975 NSCLC cells, compared to treatment with either fulvestrant or gefitinib alone; however, the molecular mechanism for the improved effects of the combination treatment are still unknown. In this study, we confirmed that fulvestrant increases the gefitinib sensitivity of H1975 cells and found that let-7c was most upregulated in the fulvestrant-treated cells. Our data revealed that let-7c increases gefitinib sensitivity by repressing RAS and inactivating the phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathways. Taken together, our findings suggest that let-7c plays an important role in fulvestrant-induced upregulation of gefitinib sensitivity in H1975 cells. [Copyright &y& Elsevier]
- Published
- 2014
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31. Soluble Beta-Amyloid Peptides, but Not Insoluble Fibrils, Have Specific Effect on Neuronal MicroRNA Expression.
- Author
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Li, Jing Jing, Dolios, Georgia, Wang, Rong, and Liao, Francesca-Fang
- Subjects
- *
AMYLOID beta-protein , *MICRORNA genetics , *GENE expression , *OLIGOMERS , *ALZHEIMER'S disease , *NEUROTOXICOLOGY , *CELL culture - Abstract
Recent studies indicate that soluble β-amyloid (sAβ) oligomers, rather than their fibrillar aggregates, contribute to the pathogenesis of Alzheimer's disease (AD), though the mechanisms of their neurotoxicity are still elusive. Here, we demonstrate that sAβ derived from 7PA2 cells exert a much stronger effect on the regulation of a set of functionally validated microRNAs (miRNAs) in primary cultured neurons than the synthetic insoluble Aβ fibrils (fAβ). Synthetic sAβ peptides at a higher concentration present comparable effect on these miRNAs in our neuronal model. Further, the sAβ-induced miR-134, miR-145 and miR-210 expressions are fully reversed by two selective N-methyl-d-aspartate (NMDA) receptor inhibitors, but are neither reversed by insulin nor by forskolin, suggesting an NMDA receptor-dependent, rather than PI3K/AKT or PKA/CREB signaling dependent regulatory mechanism. In addition, the repression of miR-107 expression by the sAβ containing 7PA2 CM is likely involved multiple mechanisms and multiple players including NMDA receptor, N-terminally truncated Aβ and reactive oxygen species (ROS). [ABSTRACT FROM AUTHOR]
- Published
- 2014
- Full Text
- View/download PDF
32. AgNPs reduce reproductive capability of female mouse for their toxic effects on mouse early embryo development.
- Author
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Zhang, Di, Yu, Fangfang, Li, Huanhuan, Wang, Qiuyue, Wang, Meiya, Qian, Hongli, Wu, Xiaoqing, Wu, Fengrui, Liu, Yong, Jiang, Shuanglin, Li, Pu, Wang, Rong, and Li, Wenyong
- Subjects
- *
GENITAL microbiology , *HUMAN reproduction , *IN vitro studies , *SILVER compounds , *ANIMAL experimentation , *FETAL development , *ANTI-infective agents , *RISK assessment , *GENE expression , *VAGINAL medication , *RESEARCH funding , *ZYGOTES , *NANOPARTICLES , *MICE , *REPRODUCTIVE health , *SILVER , *MEMBRANE potential ,RISK factors in infertility - Abstract
Silver nanoparticles (AgNPs) are widely applied in the field of personal protection for their powerful toxic effects on cells, and recently, a new type of vaginal gel with AgNPs is used to protect the female reproductive tract from microbes and viruses. However, a high risk of AgNPs to the fetus and the underlying mechanism of AgNPs to interfere in embryo development still remain unclear. Thus, this study investigated the impact of two drugs of vaginal gel with AgNPs on reproductive capability of the female mouse by animal experiment. Then, kinetics of AgNPs affecting embryo development was investigated by in vitro embryos culturing, and cell membrane potential (CMP) of zygotes was analyzed by DiBAC4(3) staining. Results indicated that one of the drugs of vaginal gel certainly injured embryo development in spite of no apparent histological change found in ovaries and uteruses of drug-treated mice. In vitro embryo culturing discovered that the toxic effect of AgNPs on embryo development presented particle sizes and dose dependent, and AgNP treatment could rapidly trigger depolarization of the cell membrane of zygotes. Moreover, AgNPs changed the gene expression pattern of Oct-4 and Cdx2 in blastocysts. All these findings suggest that AgNPs can interfere with normal cellular status including cell membrane potential, which has not been noticed in previous studies on the impact of AgNPs on mammalian embryos. Thus, findings of this study alarm us the risk of applying vaginal gel with AgNPs in individual caring and protection of the female reproductive system. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
33. AgNPs reduce reproductive capability of female mouse for their toxic effects on mouse early embryo development.
- Author
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Zhang, Di, Yu, Fangfang, Li, Huanhuan, Wang, Qiuyue, Wang, Meiya, Qian, Hongli, Wu, Xiaoqing, Wu, Fengrui, Liu, Yong, Jiang, Shuanglin, Li, Pu, Wang, Rong, and Li, Wenyong
- Subjects
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HUMAN reproduction , *IN vitro studies , *SILVER compounds , *ANIMAL experimentation , *FETAL development , *DYNAMICS , *GENE expression , *RESEARCH funding , *ZYGOTES , *NANOPARTICLES , *MICE ,RISK factors in infertility - Abstract
Silver nanoparticles (AgNPs) are widely applied in the field of personal protection for their powerful toxic effects on cells, and recently, a new type of vaginal gel with AgNPs is used to protect the female reproductive tract from microbes and viruses. However, a high risk of AgNPs to the fetus and the underlying mechanism of AgNPs to interfere in embryo development still remain unclear. Thus, this study investigated the impact of two drugs of vaginal gel with AgNPs on reproductive capability of the female mouse by animal experiment. Then, kinetics of AgNPs affecting embryo development was investigated by in vitro embryos culturing, and cell membrane potential (CMP) of zygotes was analyzed by DiBAC4(3) staining. Results indicated that one of the drugs of vaginal gel certainly injured embryo development in spite of no apparent histological change found in ovaries and uteruses of drug-treated mice. In vitro embryo culturing discovered that the toxic effect of AgNPs on embryo development presented particle sizes and dose dependent, and AgNP treatment could rapidly trigger depolarization of the cell membrane of zygotes. Moreover, AgNPs changed the gene expression pattern of Oct-4 and Cdx2 in blastocysts. All these findings suggest that AgNPs can interfere with normal cellular status including cell membrane potential, which has not been noticed in previous studies on the impact of AgNPs on mammalian embryos. Thus, findings of this study alarm us the risk of applying vaginal gel with AgNPs in individual caring and protection of the female reproductive system. [ABSTRACT FROM AUTHOR]
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- 2022
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34. Genome Wide Analysis of the Apple MYB Transcription Factor Family Allows the Identification of MdoMYB121 Gene Confering Abiotic Stress Tolerance in Plants.
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Cao, Zhong-Hui, Zhang, Shi-Zhong, Wang, Rong-Kai, Zhang, Rui-Fen, and Hao, Yu-Jin
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HUMAN genome , *MYB gene , *TRANSCRIPTION factors , *EFFECT of stress on plants , *PLANT genetics , *SECONDARY metabolism , *GENETIC engineering - Abstract
The MYB proteins comprise one of the largest families of transcription factors (TFs) in plants. Although several MYB genes have been characterized to play roles in secondary metabolism, the MYB family has not yet been identified in apple. In this study, 229 apple MYB genes were identified through a genome-wide analysis and divided into 45 subgroups. A computational analysis was conducted using the apple genomic database to yield a complete overview of the MYB family, including the intron-exon organizations, the sequence features of the MYB DNA-binding domains, the carboxy-terminal motifs, and the chromosomal locations. Subsequently, the expression of 18 MYB genes, including 12 were chosen from stress-related subgroups, while another 6 ones from other subgroups, in response to various abiotic stresses was examined. It was found that several of these MYB genes, particularly MdoMYB121, were induced by multiple stresses. The MdoMYB121 was then further functionally characterized. Its predicted protein was found to be localized in the nucleus. A transgenic analysis indicated that the overexpression of the MdoMYB121 gene remarkably enhanced the tolerance to high salinity, drought, and cold stresses in transgenic tomato and apple plants. Our results indicate that the MYB genes are highly conserved in plant species and that MdoMYB121 can be used as a target gene in genetic engineering approaches to improve the tolerance of plants to multiple abiotic stresses. [ABSTRACT FROM AUTHOR]
- Published
- 2013
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35. Leptin and HER-2 are associated with gastric cancer progression and prognosis of patients
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Geng, Yiting, Wang, Jian, Wang, Rong, Wang, Kai, Xu, Yanjie, Song, Guoxin, Wu, Changping, and Yin, Yongmei
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STOMACH cancer , *LEPTIN , *CANCER invasiveness , *GENE expression , *VASCULAR endothelial growth factors , *IMMUNOHISTOCHEMISTRY , *SOMATOMEDIN C , *PROGNOSIS - Abstract
Abstract: We conducted this study to evaluate the expression of leptin and its receptor, OB-Rb in gastric cancer and their relationship to clinicopathological features, VEGF and HER-2 expression, as well as the prognostic value. One hundred and ten gastric cancer specimens were detected for leptin, OB-Rb, VEGF and HER-2 by immunohistochemistry (IHC), and 96 specimens of normal gastric mucosa served as the control. The expression level of leptin, OB-Rb and HER-2 in gastric tissues were significantly higher than normal tissues (49.1% vs. 34.0%, 60.9% vs. 46.0%, 19.1% vs. 8.0%, P <0.05). There was a correlation between the expression of leptin and HER-2, both of which were significantly associated with invasion depth, lymph node metastasis, AJCC stage and VEGF expression. However, there was no correlation between OB-Rb expression and all clinicopathological features. Cox regression analyses showed that age, tumor size, histological grade, serosa invasion, AJCC stage, chemotherapy, leptin and HER-2 overexpression were prognostic factors. The survival of patients with leptin positive expression was significantly poorer than those with negative expression (OS: 20.0months vs. 32.5months, FPS: 12.0months vs. 18.0months, P <0.01). Leptin, rather than OB-Rb, played an important role in the progression and angiogenesis of gastric cancer, and was a prognostic factor for poor outcome. [Copyright &y& Elsevier]
- Published
- 2012
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36. Regulation of CD44 expression by tumor necrosis factor-α and its potential role in breast cancer cell migration
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Li, Jun, Zha, Xiao-Ming, Wang, Rong, Li, Xiao-Dong, Xu, Bei, Xu, Yan-Jie, and Yin, Yong-Mei
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BREAST cancer treatment , *GENE expression , *GENETIC regulation , *TUMOR necrosis factors , *CELL migration , *DRUG synergism - Abstract
Abstract: CD44 molecule plays critical role in distant malignant metastasis. It is expressed in standard form (CD44s) or variant form (CD44v). Tumor necrosis factor-α (TNF-α) is highly expressed in the cancer microenvironment. TNF-α was reported to modulate CD44 expression in several kinds of cancer. However, little is known about pathological role of TNF-α in breast cancer (BC) cells. In the current investigation, we investigated the effect of TNF-α on BC cells (MCF-7 and MDA-MB-231) viability, CD44 expression, and in vitro migration. We found that TNF-α down-regulated CD44s expression, up-regulated CD44v3 and CD44v6 expression through JNK pathway in MCF-7 cells. In MDA-MB-231 cells, TNF-α up-regulated CD44s, CD44v3 and CD44v6 expression via p38 pathway. These data indicate important role of CD44 molecule in BC pathology. [Copyright &y& Elsevier]
- Published
- 2012
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37. Inhibition of porcine reproductive and respiratory syndrome virus infection in piglets by a peptide-conjugated morpholino oligomer
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Opriessnig, Tanja, Patel, Deendayal, Wang, Rong, Halbur, Patrick G., Meng, Xiang-Jin, Stein, David A., and Zhang, Yan-Jin
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PORCINE reproductive & respiratory syndrome , *PIGLETS , *SWINE diseases , *OLIGOMERS , *ANIMAL industry , *VIRAL replication , *ANTISENSE peptides , *ANTIVIRAL agents , *GENE expression - Abstract
Abstract: Porcine reproductive and respiratory syndrome (PRRS) causes substantial economic losses to the swine industry in many countries, and current control strategies are inadequate. Previously, we explored the strategy of using peptide-conjugated phosphorodiamidate morpholino oligomers (PPMOs) to inhibit PRRS virus (PRRSV) replication. PPMOs are nuclease-resistant and single-stranded DNA analogs containing a modified backbone conjugated to a cell-penetrating peptide and can act as antisense agents through steric blockade of complementary messenger RNA. A PPMO (designated 5UP2) targeting highly conserved sequence in the 5′-terminal region of the PRRSV genome was found to produce multi-log10 inhibition of PRRSV replication in cultured cells. To evaluate 5UP2 in vivo, we here administrated the PPMO to 3-week-old piglets via intranasal instillation at 24h before, and 2 and 24h after infection with PRRSV (strain VR2385). Blood samples were collected at 6, 10 and 14days post-infection (dpi) for detection of PRRSV RNA and antibodies. Necropsy was performed at 14dpi. Monitoring weight gain in all piglet groups throughout the experiment indicated that PPMO was well tolerated at the doses used. PPMO 5UP2 treatment significantly reduced PRRSV viremia at 6dpi. On day 14, piglets receiving 5UP2 had significantly less interstitial pneumonia and lower level of anti-PRRSV antibodies than untreated piglets. In alveolar macrophages isolated at the time of necropsy, the expression of antiviral genes in PPMO-treated piglets was elevated in comparison with untreated. This study provides further data indicating that the 5UP2 PPMO can be considered a candidate component for a novel PRRS control strategy. [Copyright &y& Elsevier]
- Published
- 2011
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38. FoxO4 negatively modulates USP10 transcription to aggravate the apoptosis and oxidative stress of hypoxia/reoxygenation-induced cardiomyocytes by regulating the Hippo/YAP pathway.
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Huang, Jingwen, Liu, Yu, Wang, Mei, Wang, Rong, Ling, Huifen, and Yang, Yan
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DEUBIQUITINATING enzymes , *OXIDATIVE stress , *GENE expression , *PEPTIDASE , *MYOCARDIAL infarction , *CAUSES of death , *APOPTOSIS , *FORKHEAD transcription factors - Abstract
Acute myocardial infarction (AMI) is the main cause of death in the whole world. This study aimed to investigate whether forkhead box O4 (FoxO4) could negatively modulate ubiquitin specific peptidase 10 (USP10) transcription to aggravate the apoptosis and oxidative stress of hypoxia/reoxygenation (H/R)-induced cardiomyocytes through Hippo/YAP pathway. mRNA expression as well as protein expressions of USP10 and FoxO4 in H9C2 cells after H/R induction or transfection were respectively detected by Reverse transcription-quantitative (RT-q) PCR analysis and Western blot. The viability and apoptosis of H9C2 cells after H/R induction or transfection were respectively detected by CCK-8 and TUNEL assays. The expressions of lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in H9C2 cells after H/R induction or transfection were analyzed using appropriate kits and intracellular reactive oxygen species (ROS) levels were detected using a ROS Assay Kit. Dual luciferase reporter assay and Chromatin Immunoprecipitation (ChIP) have adopted to confirm the combination of USP10 and FoxO4. Western blot was also used to analyze the expression of apoptosis-related proteins and Hippo/YAP pathway-related proteins. As a result, USP10 expression was decreased in H/R-induced H9C2 cells in a time-dependent manner. USP10 overexpression increased the viability and suppressed the apoptosis and oxidative stress of H/R-induced H9C2 cells. In addition, FoxO4 modulated USP10 transcription. FoxO4 expression was increased in H9C2 cells induced by H/R. FoxO4 overexpression could reverse the protective effects of USP10 overexpression on H/R-induced H9C2 cells by regulating the Hippo/YAP signaling pathway. In conclusion, FoxO4 negatively modulated USP10 transcription to aggravate the apoptosis and oxidative stress of H/R-induced H9C2 cells via blocking Hippo/YAP pathway. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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39. Local injury to the endometrium in controlled ovarian hyperstimulation cycles improves implantation rates
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Zhou, Liang, Li, Rong, Wang, Rong, Huang, Hai-xiong, and Zhong, Kai
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ENDOMETRIUM , *OVARIES , *EMBRYO transfer , *GENE expression , *WOUNDS & injuries , *RNA metabolism , *BIOCHEMISTRY , *BIOPSY , *BIRTH rate , *COMPARATIVE studies , *FERTILIZATION in vitro , *LONGITUDINAL method , *PHENOMENOLOGY , *RESEARCH methodology , *MEDICAL cooperation , *INDUCED ovulation , *RESEARCH , *ULTRASONIC imaging , *EVALUATION research , *FETAL development , *RANDOMIZED controlled trials , *OLIGONUCLEOTIDE arrays , *GENE expression profiling , *PHYSIOLOGY - Abstract
Objective: To explore the possibility that local injury to the endometrium in controlled ovarian hyperstimulation cycle improves the incidence of embryo implantation and to analyze the gene expression profile in the endometria of pregnant and nonpregnant patients in in vitro fertilization/embryo transfer (IVF-ET).Design: Prospective study.Setting: A clinical assisted reproductive center of a university hospital.Patient(s): Women undergoing fresh IVF-ET cycles (n = 121), treated with a long protocol for controlled ovarian hyperstimulation, whose endometrium were diagnosed by B-ultrasound showing irregular echo.Intervention(s): Local injury to the endometrium of 60 patients in controlled ovarian hyperstimulation cycle, who were randomly selected from a total of 121 patients. Seven endometrial biopsies samples from day 10 were analyzed by Affymetrix U133 plus 2.0 gene chip.Main Outcome Measure(s): Outcomes of IVF-ET and gene expression assayed by gene chip technology.Result(s): Transfer of the same number of embryos (135 in the experimental and control patients, respectively) resulted in rates of implantation (33.33% vs. 17.78%), clinical pregnancy (48.33% vs. 27.86%), and ongoing or live births per ET (41.67% vs. 22.96%) that were higher in the experimental group compared with controls. Statistically significant differences of the expression level of 218 genes (41 up-regulated and 177 down-regulated) were detected in the endometrial biopsy samples from clinical pregnant patients and nonpregnant patients.Conclusion(s): The results suggested local injury to the endometrium during a COH cycle improved the rates of embryo implantation, clinical pregnancy and live birth in ART. We also demonstrated a statistically significant difference in the messenger RNA (mRNA) expression profiles in the endometrium of pregnant and nonpregnant patients. Further studies on the genes identified herein will assist in predicting implantation competence. [ABSTRACT FROM AUTHOR]- Published
- 2008
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40. Absolute protein expression profiling estimates the relative contributions of transcriptional and translational regulation.
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Lu, Peng, Vogel, Christine, Wang, Rong, Yao, Xin, and Marcotte, Edward M.
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PROTEOMICS , *GENE expression , *POST-translational modification , *YEAST fungi genetics , *BACTERIAL genetics , *ESCHERICHIA coli , *PEPTIDES , *MASS spectrometry - Abstract
We report a method for large-scale absolute protein expression measurements (APEX) and apply it to estimate the relative contributions of transcriptional- and translational-level gene regulation in the yeast and Escherichia coli proteomes. APEX relies upon correcting each protein's mass spectrometry sampling depth (observed peptide count) by learned probabilities for identifying the peptides. APEX abundances agree with measurements from controls, western blotting, flow cytometry and two-dimensional gels, as well as known correlations with mRNA abundances and codon bias, providing absolute protein concentrations across approximately three to four orders of magnitude. Using APEX, we demonstrate that 73% of the variance in yeast protein abundance (47% in E. coli) is explained by mRNA abundance, with the number of proteins per mRNA log-normally distributed about ∼5,600 (∼540 in E. coli) protein molecules/mRNA. Therefore, levels of both eukaryotic and prokaryotic proteins are set per mRNA molecule and independently of overall protein concentration, with >70% of yeast gene expression regulation occurring through mRNA-directed mechanisms. [ABSTRACT FROM AUTHOR]
- Published
- 2007
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41. Molecular Targets and Mechanisms of Scutellariae radix-Coptidis rhizoma Drug Pair for the Treatment of Ulcerative Colitis Based on Network Pharmacology and Molecular Docking.
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Niu, Kai, Li, Qifang, Liu, Yuan, Qiao, Yi, Li, Bingbing, Wei, Chao, Wang, Kunrui, Cui, Lu'an, Zheng, Canlei, Wang, Rong, Zhang, Li, Zhang, Honghua, Sun, Bing, and Yu, Bin
- Subjects
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ULCERATIVE colitis , *INTERLEUKINS , *LIPOPOLYSACCHARIDES , *MEDICINAL plants , *GINGER , *COMBINATION drug therapy , *PHARMACOLOGY , *MOLECULAR biology , *CELLULAR signal transduction , *GENE expression , *TUMOR necrosis factors , *MOLECULAR structure , *CHINESE medicine - Abstract
This study aims to analyze the targets of the effective active ingredients of Scutellariae radix-Coptidis rhizoma drug pair (SCDP) in ulcerative colitis (UC) by network pharmacology and molecular docking and to explore the associated therapeutic mechanism. The effective active ingredients and targets of SCDP were determined from the TCMSP database, and the drug ingredient-target network was constructed using the Cytoscape software. The disease targets related to UC were searched in GeneCards, DisGeNET, OMIM, and DrugBank databases. Then, the drug ingredient and disease targets were intersected to construct a protein-protein interaction network through the STRING database. The Metascape database was used for the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the predicted targets of SCDP for UC. The Autodock software was used for molecular docking between the main active ingredient and the core target to evaluate the binding ability. SCDP has 43 effective active ingredients and 134 intersection targets. Core targets included AKT1, TP53, IL-6, VEGFA, CASP3, JUN, TNF, MYC, EGFR, and PTGS2. GO functional enrichment analysis showed that biological process was mainly associated with a cytokine-mediated signaling pathway, response to an inorganic substance, response to a toxic substance, response to lipopolysaccharide, reactive oxygen species metabolic process, positive regulation of cell death, apoptotic signaling pathway, and response to wounding. KEGG enrichment analysis showed main pathway concentrations were related to pathways in cancer, AGE-RAGE signaling pathway in diabetic complications, bladder cancer, IL-17 signaling pathway, apoptosis, p53 signaling pathway, and PI3K-Akt signaling pathway. The drug active ingredient-core target-key pathway network contains 41 nodes and 108 edges, of which quercetin, wogonin, baicalein, acacetin, oroxylin A, and beta-sitosterol are important active ingredients; PTGS2, CASP3, TP53, IL-6, TNF, and AKT1 are important targets; and the pathways involved in UC treatment include pathways in cancer, PI3K-Akt signaling pathway, AGE-RAGE signaling pathway in diabetic, apoptosis, IL-17 signaling pathway and herpes simplex infection. The active ingredient has a good binding capacity to the core target. SCDP key active ingredients are mainly quercetin, wogonin, baicalein, acacetin, oroxylin A, and beta-sitosterol, which function mainly by regulating targets, such as PTGS2, CASP3, TP53, IL-6, TNF, and AKT1, and are associated with multiple signaling pathways as pathways in cancer, PI3K-Akt signaling pathway, apoptosis, IL-17 signaling pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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42. Urinary-derived extracellular vesicle microRNAs as non‐invasive diagnostic biomarkers for early-stage renal cell carcinoma.
- Author
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Zhang, Yu, Zhu, Yuan-Yuan, Chen, Yang, Zhang, Lele, Wang, Rong, Ding, Xiaoyu, Zhang, Huizi, Zhang, Chen-Yu, Zhang, Chunni, Gu, Wan-Jian, Wang, Cheng, and Wang, Jun-Jun
- Subjects
- *
RENAL cell carcinoma , *EXTRACELLULAR vesicles , *GENE expression , *MICRORNA , *GLOMERULAR filtration rate , *BREAST - Abstract
• Urinary extracellular vesicles miRNAs' expression pattern of RCC patients was examined. • uEV miR-135b-5p, miR-196b-5p, miR-200c-3p, and miR-203a-3p were upregulated in RCC patients. • A three-uEV miRNA panel could discriminate RCC patients from controls with the AUC of 0.785. • An uEV-miRNA panel could also distinguish early-stage RCC patients with the AUC of 0.786. The potential of urinary-derived extracellular vesicle (uEV) microRNAs (miRNAs) as noninvasive molecular biomarkers for identifying early-stage renal cell carcinoma (RCC) patients is rarely explored. The present study aims to explore the possibility of uEV miRNAs as novel molecular biomarkers for distinguishing early-stage RCC. uEVs were extracted by ExoQuick-TC™ kit and miRNA concentrations were measured by RT-qPCR. ROC curves and bioinformatics analysis were employed to predict the diagnostic efficacy and regulatory mechanisms of dysregulated miRNAs. Through a multiphase case-control study on uEV miRNAs screening, training, and validation in RCC cells (ACHN, Caki-1) and control cells (HK-2) and in uEVs of 125 RCC patients and 128 age- and sex-matched controls, we successfully identified four uEVs miRNAs (miR-135b-5p, miR-196b-5p, miR-200c-3p, and miR-203a-3p) were significantly and stably upregulated in RCC in vitro and in vivo. When adjusted with estimated glomerular filtration rate (eGFR), the AUC of the three-uEV miRNA panel (miR-135b-5p, miR-200c-3p, and miR-203a-3p) was 0.785 (95 % CI = 0.729–0.842, P < 0.0001) for discriminating RCC patients from controls. Notably, this panel exhibited similar performance in distinguishing early-stage (stage Ⅰ) RCC patients, with an AUC of 0.786 (95 %CI = 0.727–0.844, P < 0.0001). Bioinformatics analysis predicted that candidate miRNAs were involved in cancer progressing. Our study identified a four uEV miRNAs panel (miR-135b-5p, miR-196b-5p, miR-200c-3p, and miR-203a-3p) may serve as an auxiliary noninvasive indication of early-stage RCC. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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43. iMarmot: an integrative platform for comparative and functional genomics of marmots.
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Liu, Baoning, Bai, Liang, Yu, Qingqing, Hu, Fang, Wu, Jing, Zhao, Sihai, Wang, Rong, Wang, Weirong, Tao, Yuanqing, Fan, Jianglin, and Liu, Enqi
- Subjects
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FUNCTIONAL genomics , *COMPARATIVE genomics , *ANIMAL models in research , *GENE expression - Abstract
Background: Marmots are large Holarctic rodents with unique biological features, making them potential animal models in various research fields. Due to the rapid accumulation of the genetic data in marmots, a highly integrative database is urgent needed. Description: iMarmot is freely available on the web at http://www.marmotdb.org/ and currently contains the biological information of 14 marmots, genomic sequence of 6 marmots, syntenic relationship and orthologs among 3 marmots, and expression profiles of several hibernators and plague hosts. To assist with the genomic and transcriptomic analysis, we also integrated a set of analysis and visualization tools, such as KEGG or GO enrichment analysis, PCA, Blast, Muscle, GeneWise, Lastz, and JBrowse. Particularly, one DEGs (differentially expressed genes) module has been implemented in this database to visualize the gene expression changes in hibernators and plague hosts. Conclusion: This database will provide comprehensive information and analysis platform for researchers interested in understanding the biological features of marmots. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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44. A functional polymorphism in the promoter of miR-17-92 cluster is associated with decreased risk of ischemic stroke.
- Author
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Huang, Huatuo, Wei, Guijiang, Wang, Chunfang, Lu, Yulan, Liu, Chunhong, Wang, Rong, Shi, Xiang, Yang, Jun, and Wei, Yesheng
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REGULATOR genes , *GENE expression , *HAPLOTYPES , *STROKE , *PROMOTERS (Genetics) , *GENOTYPES - Abstract
Background: The microRNA-17-92 (miR-17-92) cluster is one of the most extensively studied miRNA clusters. Abnormal expression of the cluster has been found to play important role in different kinds of human diseases, including ischemic stroke (IS). The aim of our study was to investigate the association between three polymorphisms (rs1491034, rs9301654 and rs982873) in the promoter of the miR-17-92 cluster and risk of IS. Methods: Three hundred and ninety-eight patients with IS and 397 control subjects were included. The genotypes of the three polymorphisms were determined by Snapshot SNP genotyping assay. Relative expression of the cluster in peripheral blood mononuclear cells (PBMCs) of cases and controls were examined by quantitative real-time PCR. Results: Significant association between rs9301654 polymorphism and risk of IS were observed basing on genotype, model and allele analyses (GA vs. AA: adjusted OR = 0.63, 95% CI: 0.41~0.97, P = 0.037; GG vs. AA: adjusted OR = 0.23, 95% CI: 0.07~0.78, P = 0.018; GA + GG vs. AA: adjusted OR = 0.57, 95% CI: 0.38~0.87, P = 0.009; GA + AA vs. GG: adjusted OR = 0.27, 95% CI: 0.08~0.89, P = 0.032; G vs. A: adjusted OR = 0.58, 95% CI: 0.40~0.83). Haplotype analysis showed that TGC and TGT haplotypes were associated with decreased risk of IS (OR = 0.59, 95% CI: 0.40~0.87, P = 0.007 for TGC haplotype; OR = 0.21, 95% CI: 0.06~0.75, P = 0.009 for TGT haplotype). Importantly, we found the expression of miR-17-5p was significant higher while miR-19a-3p was significant lower in patient with IS compared with the control group (P < 0.01), and patients with rs9301654GG or GA genotype displayed lower level of miR-19a-3p compared with the AA genotype (P < 0.01). Conclusions: Our findings indicated that rs9301654 polymorphism in the promoter of miR-17-92 cluster may be associated with susceptibility of IS in the Chinese population. However, we found that rs9301654 polymorphism and its respective gene expression did not demonstrate consistent association with IS in the Chinese population. Further studies such as gene-gene interaction are warranted to reveal the role of miR-19a and its regulatory genes in the etiology of IS. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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45. MicroRNA‐10b expression predicts long‐term survival in patients with solid tumor.
- Author
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Zhang, Yi, Wang, Li‐Juan, Yang, He‐Quan, Wang, Rong, and Wu, Hua‐Jun
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MICRORNA , *CANCER invasiveness , *GENE expression , *CANCER prognosis , *LYMPH node cancer , *HEALTH outcome assessment - Abstract
Background: Numerous studies have evaluated the significance of the microRNA‐10b (miR‐10b) in the development and progression of many cancers. Their findings revealed that increased expression of miR‐10b is associated with unfavorable prognosis in patients with cancer. Results: A total of 1,834 patients from 19 studies were included in this study. A significantly shorter overall survival was observed in patients with increased expression of miR‐10b (hazard ratio [HR] = 1.99, 95% confidence interval [CI]: 1.51–2.61). Statistical significance was also observed in subgroup meta‐analysis stratified by the cancer type, cutoff value, analysis type, and sample size. Also, patients with a high expression level of miR‐10b had a poorer disease‐free survival rate (HR = 1.18, 95% CI: 1.05–1.33). In addition, the pooled odds ratios (ORs) showed that increased miR‐10b was also associated with positive lymph node metastasis (OR = 2.09, 95% CI: 1.45–3.03), distant metastasis (OR = 2.40, 95% CI: 1.57–3.67), tumor size (OR = 3.86, 95% CI: 2.25–6.64), and poor clinical stage (OR = 5.02, 95% CI: 3.37–7.47). Materials and Methods: A systematic literature search was conducted on a number of electronic databases, including PubMed, Embase, Web of Science, China National Knowledge Infrastructure, Springer, Google Scholar, and Gene expression omnibus. We retrieved the relevant articles to examine the association between the miR‐10b expression levels and patients' prognosis. The meta‐analysis was conducted using the RevMan 5.2 software and Stata SE12.0 software. Conclusions: High miR‐10b expression was correlated with poor clinical outcome, which indicated the potential clinical use of miR‐10b as a molecular biomarker for cancer, particularly in assessing prognosis for patients with cancers. Further studies should be performed to verify the clinical utility of miR‐10b in human solid tumors. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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46. Low temperature storage reduces aroma-related volatiles production during shelf-life of banana fruit mainly by regulating key genes involved in volatile biosynthetic pathways.
- Author
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Zhu, Xiaoyang, Luo, Jun, Li, Qiumian, Li, Jun, Liu, Tongxin, Wang, Rong, Chen, Weixin, and Li, Xueping
- Subjects
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BANANAS , *COLD storage , *VOLATILE organic compounds , *LIPOXYGENASES , *GENE expression - Abstract
Highlights • Low temperature reduced banana fruity note volatiles such as esters. • Low temperatures affected volatile-related amino acids and fatty acid compositions. • Chilling temperature affected the key enzymes and genes in volatile biosynthesis. • Low temperatures repressed the LOX pathway and amino acid metabolic pathway. Abstract Banana fruit is sensitive to chilling injury, which not only causes physical damage but also dramatically reduces fruit flavor. In this work, we evaluated the influence of non-chilling low temperature (NCT, 13 °C) and chilling temperature (CT, 5 °C) storage on volatiles production in banana in comparison to control conditions (20 °C) and evaluated the possible mechanisms. We found that CT storage caused chilling injury, which negatively affected the physical appearance of the fruit and dramatically reduced volatiles production, especially fruity note volatiles, such as esters. In contrast, NCT storage only reduced the production of a few specific volatiles. Both NCT and CT affected volatile-related amino acid and biosynthetic precursors of fatty acid compositions. The expression levels of the volatiles biosynthesis-related genes, MaHPL, MaLOX, and MaAAT, were repressed by low temperature (NCT and CT), particularly chilling temperature, while MaADH and MaPDC were up-regulated. These results suggest that CT significantly reduces volatiles production by regulating different key enzymes and genes involved in volatiles biosynthetic pathways and is mainly mediated via the repression of the lipoxygenase and amino acid metabolic pathways. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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47. Transcriptional defects and reprogramming barriers in somatic cell nuclear reprogramming as revealed by single-embryo RNA sequencing.
- Author
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Liu, Yong, Wu, Fengrui, Zhang, Ling, Wu, Xiaoqing, Li, Dengkun, Xin, Jing, Xie, Juan, Kong, Feng, Wang, Wenying, Wu, Qiaoqin, Zhang, Di, Wang, Rong, Gao, Shaorong, and Li, Wenyong
- Subjects
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SOMATIC cell nuclear transfer , *EMBRYOS , *RNA sequencing , *GENE expression , *TRANSCRIPTION factors - Abstract
Background: Nuclear reprogramming reinstates totipotency or pluripotency in somatic cells by changing their gene transcription profile. This technology is widely used in medicine, animal husbandry and other industries. However, certain deficiencies severely restrict the applications of this technology. Results: Using single-embryo RNA-seq, our study provides complete transcriptome blueprints of embryos generated by cumulus cell (CC) donor nuclear transfer (NT), embryos generated by mouse embryonic fibroblast (MEF) donor NT and in vivo embryos at each stage (zygote, 2-cell, 4-cell, 8-cell, morula, and blastocyst). According to the results from further analyses, NT embryos exhibit RNA processing and translation initiation defects during the zygotic genome activation (ZGA) period, and protein kinase activity and protein phosphorylation are defective during blastocyst formation. Two thousand three constant genes are not able to be reprogrammed in CCs and MEFs. Among these constant genes, 136 genes are continuously mis-transcribed throughout all developmental stages. These 136 differential genes may be reprogramming barrier genes (RBGs) and more studies are needed to identify. Conclusions: These embryonic transcriptome blueprints provide new data for further mechanistic studies of somatic nuclear reprogramming. These findings may improve the efficiency of somatic cell nuclear transfer. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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48. DHX29 functions as a RNA co-sensor for MDA5-mediated EMCV-specific antiviral immunity.
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Zhu, Qingyuan, Tan, Peng, Li, Yinyin, Lin, Meng, Li, Chaoran, Mao, Jingrong, Cui, Jun, Zhao, Wei, Wang, Helen Y., and Wang, Rong-Fu
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MELANOMA , *MELANOMA treatment , *CELL differentiation , *ENCEPHALOMYOCARDITIS virus , *CARRIER proteins , *PICORNAVIRUSES , *GENETICS - Abstract
Melanoma differentiation-associated gene-5 (MDA5) recognizes distinct subsets of viruses including Encephalomyocarditis virus (EMCV) of picornavirus family, but the molecular mechanisms underlying the specificity of the viral recognition of MDA5 in immune cells remain obscure. DHX29 is a RNA helicase required for the translation of 5’ structured mRNA of host and many picornaviruses (such as EMCV). We identify that DXH29 as a key RNA co-sensor, plays a significant role for specific recognition and triggering anti-EMCV immunity. We have observed that DHX29 regulates MDA5-, but not RIG-I-, mediated type I interferon signaling by preferentially interacting with structured RNAs and specifically with MDA5 for enhancing MDA5-dsRNA binding affinity. Overall, our results identify a critical role for DHX29 in innate immune response and provide molecular insights into the mechanisms by which DHX29 recognizes 5’ structured EMCV RNA and interacts with MDA5 for potent type I interferon signaling and antiviral immunity. [ABSTRACT FROM AUTHOR]
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- 2018
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49. DNA Methylation Regulates Gene Expression in Intracranial Aneurysms.
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Yu, Lanbing, Wang, Jia, Wang, Shuo, Zhang, Dong, Zhao, Yuanli, Wang, Rong, and Zhao, Jizong
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INTRACRANIAL aneurysms , *GENE expression , *DNA methylation , *GENE expression profiling , *CELL adhesion molecules , *EPIGENOMICS , *DEMETHYLATION - Abstract
Background Different gene expression profiles are observed in intracranial aneurysm tissues. Understanding these genes and what regulates their expression will provide insight into the pathogenesis of intracranial aneurysms. We investigated whether differences in DNA methylation regulate gene expression in intracranial aneurysms. Methods We compared 20 intracranial aneurysm tissue specimens with 20 matched specimens from the superficial temporal artery as controls. We identified the gene expression profiles in these samples using the GeneChip Human U133 Plus 2.0 array and evaluated DNA methylation modifications using the Infinium HumanMethylation450 BeadChip Kit. Results A total of 11,022 differentially methylated sites between aneurysm tissues and matched control tissues were identified, and 2142 differentially expressed gene transcripts were detected based on the 2 gene expression profiles. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses and verification analysis showed that the MYH11 , LIFR , and TLR4 genes were associated with the occurrence and development of intracranial aneurysms. These genes mainly encode cell adhesion molecules or are involved in the NF-κB, JAK-STAT, and ERK/JNK signaling pathways. Conclusions In the development of intracranial aneurysms, DNA methylation plays an important role in the regulation of genetic expression involved in immune and inflammatory reactions, cell function, cell maintenance, and cell signal transduction. [ABSTRACT FROM AUTHOR]
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- 2017
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50. De novo characterization of the pine aphid Cinara pinitabulaeformis Zhang et Zhang transcriptome and analysis of genes relevant to pesticides.
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Wu, Songqing, Huang, Zhicheng, Rebeca, Carballar-Lejarazú, Zhu, Xiaoli, Guo, Yajie, Lin, Qiannan, Hu, Xia, Wang, Rong, Liang, Guanghong, Guan, Xiong, and Zhang, Feiping
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CINARA , *PESTICIDES , *PINE needles , *BIOLOGICAL pest control , *GENE ontology - Abstract
The pine aphid Cinara pinitabulaeformis Zhang et Zhang is the main pine pest in China, it causes pine needles to produce dense dew (honeydew) which can lead to sooty mold (black filamentous saprophytic ascomycetes). Although common chemical and physical strategies are used to prevent the disease caused by C. pinitabulaeformis Zhang et Zhang, new strategies based on biological and/or genetic approaches are promising to control and eradicate the disease. However, there is no information about genomics, proteomics or transcriptomics to allow the design of new control strategies for this pine aphid. We used next generation sequencing technology to sequence the transcriptome of C. pinitabulaeformis Zhang et Zhang and built a transcriptome database. We identified 80,259 unigenes assigned for Gene Ontology (GO) terms and information for a total of 11,609 classified unigenes was obtained in the Clusters of Orthologous Groups (COGs). A total of 10,806 annotated unigenes were analyzed to identify the represented biological pathways, among them 8,845 unigenes matched with 228 KEGG pathways. In addition, our data describe propagative viruses, nutrition-related genes, detoxification related molecules, olfactory related receptors, stressed-related protein, putative insecticide resistance genes and possible insecticide targets. Moreover, this study provides valuable information about putative insecticide resistance related genes and for the design of new genetic/biological based strategies to manage and control C. pinitabulaeformis Zhang et Zhang populations. [ABSTRACT FROM AUTHOR]
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- 2017
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