15 results on '"Chunyan Gu"'
Search Results
2. Research progress on non-protein-targeted drugs for cancer therapy
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Yiwen Zhang, Lu Lu, Feifeng Song, Xiaozhou Zou, Yujia Liu, Xiaowei Zheng, Jinjun Qian, Chunyan Gu, Ping Huang, and Ye Yang
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Cancer Research ,Oncology - Abstract
Non-protein target drugs, especially RNA-based gene therapies for treating hereditary diseases, have been recognized worldwide. As cancer is an insurmountable challenge, no miracle drug is currently available. With the advancements in the field of biopharmaceuticals, research on cancer therapy has gradually focused on non-protein target-targeted drugs, especially RNA therapeutics, including oligonucleotide drugs and mRNA vaccines. This review mainly summarizes the clinical research progress in RNA therapeutics and highlights that appropriate target selection and optimized delivery vehicles are key factors in increasing the effectiveness of cancer treatment in vivo.
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- 2023
3. G6PD promotes cell proliferation and dexamethasone resistance in multiple myeloma via increasing anti-oxidant production and activating Wnt/β-catenin pathway
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Rui, Li, Mengying, Ke, Mingming, Qi, Zhenru, Han, Yuhao, Cao, Zhendong, Deng, Jinjun, Qian, Ye, Yang, and Chunyan, Gu
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Cancer Research ,Oncology ,Hematology - Abstract
Background Glucose-6-phosphate dehydrogenase (G6PD) as the rate-limiting enzyme in the pentose phosphate pathway (PPP) is well-established as an aberrantly expressed protein in numerous clinical diseases; however, its role in cancer, specifically in multiple myeloma (MM) remains elusive. Methods In this study, serum metabolites in 70 normal people and 70 newly diagnosed MM patients were analyzed using untargeted metabolomics and the results were verified using ELISA. The survival analysis of multiple clinical datasets was performed to identify a potential target gene in MM. The oncogenic role of G6PD was investigated using lentivirus-based overexpression or knockdown of G6PD using RNAi or an inhibitor in vitro, and in a xenograft mouse model in vivo. The mechanisms of induced Dexamethasone (Dexa)-resistance of G6PD were further explored using the above established MM cell lines in vitro. Results Based on the screening of potential genes, PPP was shown to be involved in the occurrence of MM, which was evidenced by the differential expression of serum metabolites of G6P and Dehydroepiandrosterone sulfate (DHEAS, the more stable sulfate ester form of an endogenously uncompetitive G6PD inhibitor known as DHEA). Elevated G6PD promoted MM cell proliferation. Mechanistically, high G6PD expression enhanced enzymatic generation of the antioxidant NADPH via the PPP and decreased the production of reactive oxygen species (ROS), thus inducing the proliferation and Dexa resistance in MM cells. Furthermore, canonical Wnt/β-catenin signaling also participated in regulating G6PD-induced drug resistance and cellular redox levels of ROS. Intriguingly, DHEA treatment could enhance the sensitivity of MM cells to Dexa primarily through augmenting cellular oxidative stress. Conclusions Our data demonstrate that G6PD enhances the generation of the enzymatic anti-oxidant NADPH and decreases ROS generation, thereby promoting resistance to Dexa-induced apoptosis via the enzymatic PPP and non-enzymatic Wnt/β-catenin signaling pathway in MM. Targeting G6PD to harness cellular redox may serve as a promising novel strategy for the management of MM.
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- 2022
4. Elevated SFXN2 limits mitochondrial autophagy and increases iron-mediated energy production to promote multiple myeloma cell proliferation
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Ying Chen, Jinjun Qian, Pinggang Ding, Wang Wang, Xinying Li, Xiaozhu Tang, Chao Tang, Ye Yang, and Chunyan Gu
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Cancer Research ,Iron ,Immunology ,Membrane Proteins ,Cell Biology ,Antioxidants ,Mitochondria ,Cellular and Molecular Neuroscience ,Autophagy ,Humans ,Multiple Myeloma ,Cation Transport Proteins ,Heme Oxygenase-1 ,Cell Proliferation - Abstract
Human sideroflexin 2 (SFXN2) belongs to the SFXN protein family, which is a mitochondrial outer membrane protein involved in mitochondrial iron metabolism. Mitochondria are indispensable for cellular energy production and iron metabolism. However, it remains elusive how SFXN2 modulates mitochondrial homeostasis and cellular iron metabolism in multiple myeloma (MM). In this study, we first found that SFXN2 was significantly elevated and correlated to poor outcomes in MM patients from clinical datasets. SFXN2 overexpression promoted MM cell proliferation and suppressed starvation-induced autophagy/mitophagy, while SFXN2 knockdown aggravated mitochondria damage and autophagic processes in ARP1 and H929 MM cell lines. Furthermore, inhibition of SFXN2 exerted effectively anti-myeloma activity in vivo by using myeloma xenograft model. Mechanism studies indicated that heme oxygenase 1 (HO1) with anti-oxidant function contributed to the process of autophagy suppression and cellular proliferation mediated by SFXN2. Our study revealed the critical role of SFXN2 in regulating mitochondrial bioenergetics, mitophagy, cellular iron metabolism, and redox homeostasis in interconnected and intricate way. Collectively, these findings not only provide insights into the metabolic reprogramming of tumor cells, but also highlight the therapeutic potential of SFXN2 in combination with iron metabolism as target for prognosis and treatment in MM patients.
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- 2022
5. New Spectral Classification Index for Rapid Identification of Fusarium Infection in Wheat Kernel
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Gao Chen, Ling Zheng, Fenfang Lin, Qian Wang, Lei Yu, Dongyan Zhang, Shizhuang Weng, and Chunyan Gu
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Gaussian ,Stellar classification ,01 natural sciences ,Applied Microbiology and Biotechnology ,Analytical Chemistry ,symbols.namesake ,0404 agricultural biotechnology ,Histogram ,Gaussian function ,Sensitivity (control systems) ,Safety, Risk, Reliability and Quality ,Mathematics ,Intersection (set theory) ,business.industry ,010401 analytical chemistry ,Hyperspectral imaging ,Pattern recognition ,04 agricultural and veterinary sciences ,040401 food science ,0104 chemical sciences ,Kernel (statistics) ,symbols ,Artificial intelligence ,business ,Safety Research ,Food Science - Abstract
Fusarium-damaged kernels (FDK) contain a wide spectrum of mycotoxins, affecting the quality and safety of wheat used as food and feed. At present, traditional methods to detect FDK are time-consuming and laborious. Therefore, we propose herein a new spectral classification index (NSCI) method that can provide simple and low-cost FDK detection by analysing spectra in the wavelength range 350–2500 nm. The proposed index was based on the spectral reflectance and its first derivative. Frequency histograms were plotted for each class of index value, and Gaussian curve fitting was carried out for each histogram. Wheat kernels were then classified by using the intersection of the Gaussian curves as a threshold. The classification of NSCI for spectral data obtained the detection accuracy of 0.97, with a specificity of 0.99, a sensibility of 0.93 and a training time of 15.07 s. Compared with other spectral indexes and machine learning methods, the NSCI was more equilibrated in terms of efficiency and accuracy. Meanwhile, the threshold could be tuned to adjust accuracy, sensitivity or specificity to satisfy different practical needs. We also applied the NSCI for kernel hyperspectral data in another year, and the classification results is promising. The proposed method has the potential for the rapid and simple detection of FDK in wheat.
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- 2020
6. Activation of BDNF-AS/ADAR/p53 Positive Feedback Loop Inhibits Glioblastoma Cell Proliferation
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Xinwen Lv, Chunyan Gu, and Shiwen Guo
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0301 basic medicine ,Transcription, Genetic ,Adenosine Deaminase ,RNA Stability ,Down-Regulation ,Biology ,Biochemistry ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Downregulation and upregulation ,Transcription (biology) ,Cell Line, Tumor ,Humans ,RNA, Messenger ,Transcription factor ,Cell Proliferation ,Messenger RNA ,Cell growth ,RNA-Binding Proteins ,General Medicine ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Cell culture ,Apoptosis ,ADAR ,Cancer research ,RNA, Long Noncoding ,Tumor Suppressor Protein p53 ,Glioblastoma ,030217 neurology & neurosurgery - Abstract
Despite progress in conventional treatment for glioblastoma (GBM), the prognosis remains poor due to high tumor recurrence. Therefore, identification of new molecular mechanisms is a pressing need for betterment of GBM patient outcomes. qRT-PCR was used to determine BDNF-AS expression in GBM cells. CCK-8, EdU incorporation, and caspase-3 activity assays were employed to analyze biological functions of BDNF-AS. RIP and RNA pull-down were conducted to detect the interactions among BDNF-AS, ADAR, and p53. Actinomycin D was utilized to examine the stability of p53 mRNA. ChIP and luciferase reporter assays were performed to detect transcriptional activation of BDNF-AS by p53. We found that BDNF-AS was significantly downregulated in GBM cell lines, and its overexpression inhibited GBM cell growth, and promoted apoptosis. Importantly, we illustrated that BDNF-AS coupled with ADAR protein to potentiate stability of p53 mRNA and thus upregulate p53. Interestingly, we further identified p53 as a transcription factor of BDNF-AS, activating transcription of BNDF-AS. This study firstly demonstrated that BDNF-AS acted as a tumor suppressor in GBM and the positive feedback circuit of BDNF-AS/ADAR/p53 served an important mechanism to control GBM proliferation. Targeting this auto-regulatory loop may provide a potential therapeutic strategy for GBM patients.
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- 2020
7. BUB1B and circBUB1B_544aa aggravate multiple myeloma malignancy through evoking chromosomal instability
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Pinggang Ding, Mengjie Guo, Ye Yang, Xiaosong Gu, Mengying Ke, Zhendong Deng, Xiaozhu Tang, Muxi Li, Zigen Lin, Chunyan Gu, Yuxia Yuan, and Yanyan Zhou
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Male ,Cancer Research ,QH301-705.5 ,Cell Cycle Proteins ,Protein Serine-Threonine Kinases ,Plasma cell ,BUB1B ,Malignancy ,Disease-Free Survival ,Article ,Non-coding RNAs ,Mice ,In vivo ,Cell Line, Tumor ,Chromosomal Instability ,Chromosome instability ,Genetics ,medicine ,Animals ,Humans ,Biology (General) ,RNA, Small Interfering ,Multiple myeloma ,Cell Proliferation ,Haematological cancer ,Chemistry ,Kinase ,RNA, Circular ,Prognosis ,medicine.disease ,Gene Expression Regulation, Neoplastic ,medicine.anatomical_structure ,Cancer research ,Medicine ,Heterografts ,Female ,Bone marrow ,Neoplasm Recurrence, Local ,Multiple Myeloma - Abstract
Multiple myeloma (MM) is an incurable plasma cell malignancy in the bone marrow characterized by chromosome instability (CIN), which contributes to the acquisition of heterogeneity, along with MM progression, drug resistance, and relapse. In this study, we elucidated that the expression of BUB1B increased strikingly in MM patients and was closely correlated with poor outcomes. Overexpression of BUB1B facilitated cellular proliferation and induced drug resistance in vitro and in vivo, while genetic targeting BUB1B abrogated this effect. Mechanistic studies unveiled that enforced expression of BUB1B evoked CIN resulting in MM poor outcomes mainly through phosphorylating CEP170. Interestingly, we discovered the existence of circBUB1B_544aa containing the kinase catalytic center of BUB1B, which was translated by a circular RNA of BUB1B. The circBUB1B_544aa elevated in MM peripheral blood samples was closely associated with MM poor outcomes and played a synergistic effect with BUB1B on evoking CIN. In addition, MM cells could secrete circBUB1B_544aa and interfere the MM microenvironmental cells in the same manner as BUB1B full-length protein. Intriguingly, BUB1B siRNA, targeting the kinase catalytic center of both BUB1B and circBUB1B_544aa, significantly inhibited MM malignancy in vitro and in vivo. Collectively, BUB1B and circBUB1B_544aa are promising prognostic and therapeutic targets of MM.
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- 2021
8. Alternative splicing and cancer: a systematic review
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Chunyan Gu, Yuanjiao Zhang, Ye Yang, and Jinjun Qian
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0301 basic medicine ,Cancer Research ,RNA splicing ,Carcinogenesis ,medicine.medical_treatment ,lcsh:Medicine ,Drug development ,Review Article ,Biology ,medicine.disease_cause ,Non-coding RNAs ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,Cancer immunotherapy ,Neoplasms ,Genetics ,medicine ,Humans ,lcsh:QH301-705.5 ,Molecular medicine ,lcsh:R ,Alternative splicing ,Cancer ,RNA ,RNA, Circular ,medicine.disease ,Gene Expression Regulation, Neoplastic ,Alternative Splicing ,030104 developmental biology ,lcsh:Biology (General) ,Tumor progression ,030220 oncology & carcinogenesis ,Cancer research ,RNA Splicing Factors - Abstract
The abnormal regulation of alternative splicing is usually accompanied by the occurrence and development of tumors, which would produce multiple different isoforms and diversify protein expression. The aim of the present study was to conduct a systematic review in order to describe the regulatory mechanisms of alternative splicing, as well as its functions in tumor cells, from proliferation and apoptosis to invasion and metastasis, and from angiogenesis to metabolism. The abnormal splicing events contributed to tumor progression as oncogenic drivers and/or bystander factors. The alterations in splicing factors detected in tumors and other mis-splicing events (i.e., long non-coding and circular RNAs) in tumorigenesis were also included. The findings of recent therapeutic approaches targeting splicing catalysis and splicing regulatory proteins to modulate pathogenically spliced events (including tumor-specific neo-antigens for cancer immunotherapy) were introduced. The emerging RNA-based strategies for the treatment of cancer with abnormally alternative splicing isoforms were also discussed. However, further studies are still required to address the association between alternative splicing and cancer in more detail.
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- 2021
9. CCN1 promotes hepatic steatosis and inflammation in non-alcoholic steatohepatitis
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Yan Sun, Zhaolian Bian, Linling Ju, Chunyan Gu, Hong Xue, Xiong Ma, Jian-Guo Shao, Lin Chen, Jue Wei, Xi Luo, and Rujian Lu
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Adult ,Male ,Gastrointestinal Diseases ,lcsh:Medicine ,Mice, Obese ,Apoptosis ,Inflammation ,Article ,Mice ,Gastrointestinal cancer ,chemistry.chemical_compound ,Downregulation and upregulation ,Non-alcoholic Fatty Liver Disease ,Fibrosis ,Cell Adhesion ,medicine ,Animals ,Humans ,lcsh:Science ,chemistry.chemical_classification ,Multidisciplinary ,Fatty acid metabolism ,lcsh:R ,Fatty liver ,Fatty acid ,Middle Aged ,Lipid Metabolism ,medicine.disease ,Fatty Liver ,Mice, Inbred C57BL ,Liver ,chemistry ,Hepatocytes ,Cancer research ,Cytokines ,lcsh:Q ,Female ,Steatosis ,Steatohepatitis ,medicine.symptom ,Cysteine-Rich Protein 61 - Abstract
Non-alcoholic fatty liver disease (NAFLD) is characterized by increased uptake and accumulation of lipids in hepatocytes. Simple steatosis may progress to non-alcoholic steatohepatitis (NASH) with inflammation, hepatocellular injury and fibrosis. CCN1 is an important matrix protein that regulates cell death and promotes immune cell adhesion and may potentially control this process. The role of CCN1 in NASH remains unclear. We investigated the role of CCN1 in the pathogenesis of steatohepatitis. CCN1 upregulation was found to be closely related with steatosis in patients with NASH, obese mice and a FFA-treated hepatocyte model. Controlling the expression of CCN1 in murine NASH models demonstrated that CCN1 increased the severity of steatosis and inflammation. From the sequence results, we found that fatty acid metabolism genes were primarily involved in the MCD mice overexpressing CCN1 compared to the control. Then, the expression of fatty acid metabolism genes was determined using a custom-designed pathway-focused qPCR-based gene expression array. Expression analysis showed that CCN1 overexpression significantly upregulated the expression of fatty acid metabolism-associated genes. In vitro analysis revealed that CCN1 increased the intracellular TG content, the pro-inflammatory cytokines and the expression level of apoptosis-associated proteins in a steatosis model using murine primary hepatocytes. We identified CCN1 as an important positive regulator in NASH.
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- 2020
10. Age-related changes in the BACH2 and PRDM1 genes in lymphocytes from healthy donors and chronic lymphocytic leukemia patients
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Mohammad Krayem, Vu Luan Dang Chi, Soizic Garaud, Karen Willard-Gallo, Catherine Sibille, Mimoune Berehad, Chunyan Gu-Trantien, Jean Nicolas Lodewyckx, Hugues Duvillier, Pushpamali De Silva, Vincent Thibaud, Dominique Bron, and Basile Stamatopoulos
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Male ,0301 basic medicine ,Aging ,Cancer Research ,Chronic lymphocytic leukemia ,Apoptosis ,BACH2 ,0302 clinical medicine ,hemic and lymphatic diseases ,Gene expression ,Positive Regulatory Domain I-Binding Factor 1 -- genetics -- immunology -- metabolism ,Lymphocytes ,Cellular Senescence ,Aged, 80 and over ,biology ,Lymphocyte Subsets -- immunology -- metabolism ,Immunosenescence ,Middle Aged ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Healthy Volunteers ,Up-Regulation ,Cellular Senescence -- immunology ,Basic-Leucine Zipper Transcription Factors ,Real-time polymerase chain reaction ,Oncology ,030220 oncology & carcinogenesis ,Female ,Untreated Chronic Lymphocytic Leukemia ,Research Article ,Adult ,Down-Regulation -- immunology ,Down-Regulation ,lcsh:RC254-282 ,CD19 ,Young Adult ,03 medical and health sciences ,PRDM1 ,Genetics ,medicine ,Humans ,RNA, Messenger ,Aged ,Leukemia, Lymphocytic, Chronic, B-Cell -- blood -- immunology -- pathology ,medicine.disease ,Leukemia, Lymphocytic, Chronic, B-Cell ,RNA, Messenger -- metabolism ,Up-Regulation -- immunology ,Lymphocyte Subsets ,Aging -- immunology ,030104 developmental biology ,Basic-Leucine Zipper Transcription Factors -- genetics -- immunology -- metabolism ,Immunology ,biology.protein ,Positive Regulatory Domain I-Binding Factor 1 ,CD8 ,Hématologie - Abstract
Age-related genetic changes in lymphocyte subsets are not currently well documented. BACH2 is a transcription factor that plays an important role in immune-mediated homeostasis by tightly regulating PRDM1 expression in both B-cells and T-cells. BACH2 gene expression is highly sensitive to DNA damage in aged mice. This concept led us to investigate the variation in BACH2 and also PRDM1 expression in major lymphocyte subsets with age., info:eu-repo/semantics/published
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- 2019
11. Upregulation of FOXM1 in a subset of relapsed myeloma results in poor outcome
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Anja Seckinger, Siegfried Janz, Ye Yang, Carol J. Holman, Ramakrishna Sompallae, Guido Tricot, Fenghuang Zhan, Chunyan Gu, Xuefang Jing, Hartmut Goldschmidt, Dirk Hose, Michael H. Tomasson, Hematology, and Basic (bio-) Medical Sciences
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Male ,0301 basic medicine ,Oncology ,medicine.medical_specialty ,MEDLINE ,UP-REGULATION ,lcsh:RC254-282 ,Outcome (game theory) ,Pathology and Forensic Medicine ,03 medical and health sciences ,0302 clinical medicine ,Text mining ,Forkhead Box Protein M1/biosynthesis ,Downregulation and upregulation ,Recurrence ,Internal medicine ,Correspondence ,Humans ,Medicine ,Neoplasm Proteins/biosynthesis ,Multiple myeloma ,Regulation of gene expression ,Multiple Myeloma/metabolism ,business.industry ,Forkhead Box Protein M1 ,Follow up studies ,Hematology ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,medicine.disease ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,030220 oncology & carcinogenesis ,FOXM1 ,Female ,Multiple Myeloma ,business ,Follow-Up Studies - Published
- 2018
12. miR-383 inhibits hepatocellular carcinoma cell proliferation via targeting APRIL
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Guan Haitao, Feng Wang, Chunyan Gu, Jianguo Shao, Lin Chen, and Yali Cao
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Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Cell cycle checkpoint ,Tumor Necrosis Factor Ligand Superfamily Member 13 ,Down-Regulation ,Apoptosis ,Kaplan-Meier Estimate ,Biology ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,microRNA ,medicine ,Humans ,RNA, Messenger ,neoplasms ,Cell Proliferation ,Cell growth ,Liver Neoplasms ,Hep G2 Cells ,General Medicine ,Middle Aged ,Cell cycle ,Prognosis ,medicine.disease ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,030104 developmental biology ,Cell culture ,Tumor progression ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Cancer research ,Female - Abstract
Mounting evidence has shown that microRNAs (miRNAs), a class of small non-coding RNAs, are frequently deregulated in human malignancies and have pivotal roles in diverse biological processes including cancer cell proliferation. Herein, we investigated the expression pattern of miR-383 in 64 hepatocellular carcinoma (HCC) tissues and 4 HCC cell lines and found that miR-383 was downregulated in HCC tissues and cell lines. Moreover, miR-383 expression in HCC was significantly correlated with tumor size and tumor-node-metastasis (TNM) stage. Kaplan-Meier analysis showed that decreased miR-383 expression was associated with poor overall survival of HCC patients. In addition, Cox regression analysis indicated that miR-383 was an independent prognostic factor for HCC patients. Then, functional studies demonstrated that ectopic miR-383 expression could significantly suppress the in vitro proliferation of HCC cells, as well as induce cell cycle arrest and cell apoptosis. Luciferase reporter assay further identified that a proliferation-inducing ligand (APRIL), a member in the tumor necrosis factor (TNF) superfamily, was a novel target gene for miR-383. Subsequent investigation revealed that miR-383 expression was inversely correlated with APRIL messenger RNA (mRNA) expression in HCC tissues. Besides, recombinant human APRIL (rhAPRIL) could rescue HCC cell proliferation inhibited by miR-383. Taken together, our present study provided the first evidence that miR-383 was decreased in HCC and associated with tumor progression and prognosis of HCC patients. Furthermore, our findings confirmed that miR-383 might inhibit HCC cell proliferation partially via downregulating APRIL expression. Thus, this study might provide a promising strategy by targeting with the miR-383-APRIL axis in the treatment of HCC.
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- 2015
13. Correlates and Mediators of Problem Behaviors Among Children Affected by HIV/AIDS in Rural China: A Structural Equation Modeling Analysis
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Junfeng Zhao, Xiaoming Li, Chunyan Gu, Guoxiang Zhao, and Qun Zhao
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Prevention intervention ,medicine.disease ,Structural equation modeling ,Developmental psychology ,Social support ,Acquired immunodeficiency syndrome (AIDS) ,Developmental and Educational Psychology ,medicine ,School adjustment ,Future orientation ,Life-span and Life-course Studies ,China ,Psychology ,Psychosocial ,Clinical psychology - Abstract
The current study examines the relationships of several psychosocial correlates and mediating factors with problem behaviors among children (6–18 years of age) affected by parental HIV/AIDS in rural China. Cross-sectional data were collected from 755 children orphaned by AIDS (“orphans”) and 466 children living with HIV-positive parents (“vulnerable children”) during 2006–2007 in central rural China. The structural equation modeling analyses revealed that HIV-related stigma had a positive direct effect on problem behaviors of vulnerable children, while HIV-related stigma and low education aspiration had direct negative effects on school adjustment among both orphans and vulnerable children. Measures of future orientation and perceived social support mediated the effect of HIV-related stigma and low education aspiration on school adjustment, which in turn was negatively associated with problem behaviors of both groups. The data also showed that school adjustment mediated the effect of low education aspiration and HIV-related stigma on problem behaviors of both orphans and vulnerable children. Future prevention intervention efforts aiming to reduce problem behaviors and improve school adjustment among these children should target multiple factors at individual, community, and societal levels such as enhancing the children’s future expectation, increasing the social support from family, school, and community, and reducing HIV-related stigma against children and families affected by HIV.
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- 2014
14. Biocontrol of bacterial soft rot of calla lily by elicitor HarpinXoo and N-acyl homoserine lactonase (AttM)
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Fengquan Liu, Guoliang Qian, Baishi Hu, Yue-Jing Kang, Jiaqin Fan, Xue Yang, Yao Ma, and Chunyan Gu
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biology ,Physiology ,Homoserine ,food and beverages ,Pectobacterium carotovorum ,General Medicine ,Agrobacterium tumefaciens ,biology.organism_classification ,Applied Microbiology and Biotechnology ,Plant disease ,Microbiology ,Elicitor ,Bacterial soft rot ,chemistry.chemical_compound ,Xanthomonas oryzae ,chemistry ,Lactonase ,biology.protein ,Biotechnology - Abstract
Bacterial soft rot caused by Pectobacterium carotovorum subsp. carotovorum is a serious plant disease in Zantedeschia spp. (also called calla lily). In this study, two independent genes (a N-acyl homoserine lactonase gene attM from Agrobacterium tumefaciens and a hypersensitive response and pathogenicity gene hrf1 from Xanthomonas oryzae pv. oryzae), transcribed by a strong and constitutive Escherichia coli promoter Plpp, respectively, were cloned into plasmid pUC19, and was transformed into E. coli, creating strain JM109/pPHA. The result of sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS–PAGE) assay showed that both genes (hrf1 and attM) were successfully expressed in one plasmid system in strain JM109/pPHA. The expressed HarpinXoo (Hrf1) and AttM protein had the ability of inducing hypersensitive response (HR) in nonhost tobacco and degrading the N-acyl homoserine lactones (AHLs) produced by P. carotovorum subsp. carotovorum, respectively, whereas HarpinXoo and AttM protein did not seem to interfere with the normal growth of this pathogen. In planta, strain JM109/pPHA could significantly reduce the soft rot disease severity on dormant tubers (control efficiency: 92.8%) or potted plants (control efficiency: 92.4%) of calla lily. We have first demonstrated the both biocontrol effects of HarpinXoo and AttM proteins (also described as Quorum interference) on the bacterial soft rot disease of calla lily, caused by P. carotovorum subsp. carotovorum. This work provided a potential way to control this serious plant disease.
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- 2010
15. [Untitled]
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Tony Soares, Inhou Chu, Roger J. Smith, I.Y. Rosenblum, George Mandakas, Jairam Palamanda, Federico M Goodsaid, Zhiling Li, Kevin B. Alton, Laura Norton, Chunyan Gu, Diana Montgomery, Narendra S. Kishnani, and Xiaoli You
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Pharmacology ,biology ,medicine.diagnostic_test ,Organic Chemistry ,Pharmaceutical Science ,Cytochrome P450 ,Molecular biology ,Enzyme assay ,Blot ,Reverse transcription polymerase chain reaction ,Real-time polymerase chain reaction ,Western blot ,In vivo ,Gene expression ,biology.protein ,medicine ,Molecular Medicine ,Pharmacology (medical) ,Biotechnology - Abstract
Purpose. A conventional approach to assess cytochrome P450 (CYP) induction in preclinical animal models involves daily dosing for a least a week followed by Western blot and/or enzyme activity analysis. To evaluate the potential benefit of a third more specific and sensitive assay, real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), with the objective of reducing the duration of the conventional 1-week study, we simultaneously assessed gene expression by qRT-PCR along with Western blots and enzyme activity assays as a time course in an in vivo model.
- Published
- 2003
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