31 results on '"Zhongheng Wei"'
Search Results
2. Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qiang Qin, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
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Breast cancer stem cells ,LINC00511 ,E2F1 ,Nanog ,miR-185-3p ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Emerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism. Methods The lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding. Results LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription. Conclusion In conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them.
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- 2018
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3. RETRACTED: Circular RNA hsa_circ_0013958 Functions as an Oncogenic Gene Through Modulating miR-532-3p/WEE1 Axis in Hepatocellular Carcinoma
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Tao Ma, Yue Ma, Yongjun Du, Zhongheng Wei, Jianchu Wang, Yufu Jun, and Fenqiang Xiao
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hepatocellular carcinoma ,circ0013958 ,miR-532-3p ,WEE1 ,ceRNA ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Backgroundcirc0013958 was identified as a biomarker, which can be used for the diagnosis and screening of lung cancer. However, the role of circ0013958 in hepatocellular carcinoma (HCC) remains unclear.MethodsIn our study, quantitative real-time polymerase chain reaction was performed to determine the levels of circ0013958 in HCC tissues and cell lines. EdU, CCK-8, transwell, flow cytometry and tumorigenesis assays were applied to assess the functions of circ0013958 in HCC in vitro and in vivo. Western blot assay was to detect the expression of WEE1. Luciferase reporter assay, bioinformatics analysis and rescue experiments were used to examine the interaction among circ0013958, miR-532-3p and WEE1.ResultsIt revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients. Circ0013958 promoted HCC cell proliferation and invasion, inhibited cell apoptosis in vitro, and promoted tumorigenesis in vivo. Circ0013958 acted as a miR-532-3p sponge to regulate WEE1 expression, thus promoting the progression of HCC.ConclusionsCirc0013958 promotes HCC progression through miR-532-3p/WEE1 axis. Circ0013958 may serve as a potential diagnostic biomarker and therapeutic target of HCC.
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- 2021
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4. Co-expressing LRP6 With Anti-CD19 CAR-T Cells for Improved Therapeutic Effect Against B-ALL
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Ping He, Zhongqiu Tan, Zhongheng Wei, Cheng-Liang Wan, and Shan-Shan Yang
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tumor immunotherapy ,CAR-T cells ,T memory cell ,B-cell acute lymphocytic leukemia ,tumor treatment ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
BackgroundCellular immunotherapies, such as chimeric antigen receptor modified-T cell (CAR-T) therapy, offers excellent potential for tumor treatment. The memory phenotype of CAR-T has been correlated positively with a therapeutic effect on and prognosis of cancer.MethodThe proliferation rates of novel CAR-T was determined by cell counting. The phenotypes of CAR-T cells were then detected by flow cytometry. The cell cytotoxicity against tumor cells in vitro was investigated by lactate dehydrogenase assay and luciferase assay. The cytokines secreted during these assays were determined by the cytometric bead array assay. The antitumor ability in vivo was evaluated in NOG mice.ResultsCo-expression of an LRP6 full-length protein with anti-CD19 CAR significantly improved the memory phenotype of CAR-positive T-cells by enhancing the wnt signaling pathway. As compared with anti-CD19 CAR-T, anti-CD19 CAR-T-LRP6 exhibited more robust cytotoxicity against tumor cells in vitro and in vivo, albeit fewer cytokines were released in vitro. Moreover, the longer survival rate and robust expansion in vivo of anti-CD19 CAR-T-LRP6 cells were found to be effective in inhibiting cancer recurrence.ConclusionsCAR co-expressed with LRP6 could sustain the memory phenotype that enabled permanent relief and may further assist in the development of potent and durable T-cell therapeutics.
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- 2020
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5. Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury
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Lanqing Meng, Qing Huang, Xuebin Li, Ping Liang, Yueyong Li, Xiaohua Huang, Jingjie Zhao, Qiuping Chen, Rong Qiu, Lan Li, Chongdong Jian, Hongfei Yao, Jianmin Huang, Xionglin Tang, Zechen Wang, Zhongheng Wei, Jun Wu, Liuzhi Wei, Qiuju Wei, Qianli Tang, Lu Huang, Jihua Wei, Dinggui Lu, Qunqiang Luo, Kegong Xie, Yang Ouyang, Jian Chen, Genliang Li, Linxue Luo, Linbo He, Chenyi Zhuo, Anding Xu, and Lingzhang Meng
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN’s neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.
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- 2020
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6. RETRACTED ARTICLE: Isoginkgetin attenuates endoplasmic reticulum stress-induced autophagy of brain after ischemic reperfusion injury
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Lingzhang Meng, Dong Li, Yingning Wu, Xuebin Li, Xiaohua Huang, Baosheng Li, Yueyong Li, Cheng Lin, Shaocai Qiu, Deyou Huang, and Zhongheng Wei
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Kinase ,Chemistry ,ATF6 ,Endoplasmic reticulum ,Autophagy ,Ischemia ,Bioengineering ,General Medicine ,Tunicamycin ,Pharmacology ,medicine.disease ,Applied Microbiology and Biotechnology ,chemistry.chemical_compound ,Unfolded protein response ,medicine ,Protein kinase A ,Biotechnology - Abstract
Isoginkgetin is characterized by properties of potent anticancer and anti-inflammation. To explore its effect on ischemic stroke, a rat model of ischemia/reperfusion (I/R) injury was established and induced by transient middle cerebral artery occlusion/reperfusion (MCAO/R). Different doses of isoginkgetin were intraperitoneally injected into each rat. Expressions of ER stress activation-related makers including phosphorylated inositol-requiring enzyme 1 (IRE1), phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), activating transcription factor-6 (ATF6), and two autophagy markers (ratio of LC3II/I and Beclin-1) were detected by western blot. Infarct volume, neurological deficits, and brain water content were detected. The results showed that ER stress and autophagy were activated by cerebral (I/R) injury, which could be effectively attenuated following pre-ischemia isoginkgetin administration. Moreover, autophagy induced by ER stress was triggered by the activation of PERK and IRE1 pathways. ER stress inhibitor (4-PBA) and ER related signaling inhibitors including PERK, GSK, IRE1, and DBSA markedly inhibited ER stress and autophagy induced by I/R. In addition, isoginkgetin markedly mitigated cerebral infarction, edema, neuronal apoptosis as well as neurological impairment induced by I/R injury, while tunicamycin (ER stress activator TM) and rapamycin (autophagy activator RAPA) could eliminate these lesions. This research identified a novel therapeutic agent isoginkgetin, which could effectively attenuate I/R injury by blocking autophagy induced by ER stress.
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- 2022
7. A putative competing endogenous RNA network in cisplatin-resistant lung adenocarcinoma cells identifying potentially rewarding research targets
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Zhongheng Wei, Shiqing Huang, Bo Yang, and Yepeng Li
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0301 basic medicine ,Cisplatin ,Cancer Research ,Oncogene ,Competing endogenous RNA ,Articles ,bioinformatics ,Cell cycle ,Biology ,medicine.disease ,lung adenocarcinoma ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Oncology ,030220 oncology & carcinogenesis ,Gene expression ,microRNA ,medicine ,Cancer research ,Adenocarcinoma ,competing endogenous RNA ,cisplatin resistance ,Gene ,medicine.drug - Abstract
Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer and has a poor 5 year survival rate (
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- 2020
8. lncRNA HOXB‐AS3 exacerbates proliferation, migration, and invasion of lung cancer via activating the PI3K‐AKT pathway
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Zhongheng Wei, Wenyang Jiang, Wei Wang, Donghang Li, Jindan Kai, and Ying Wang
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Male ,0301 basic medicine ,Lung Neoplasms ,Physiology ,Clinical Biochemistry ,Cell ,Mice, Nude ,Biology ,medicine.disease_cause ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,0302 clinical medicine ,Cell Movement ,Carcinoma, Non-Small-Cell Lung ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Neoplasm Invasiveness ,RNA, Antisense ,RNA, Small Interfering ,Lung cancer ,Protein kinase B ,PI3K/AKT/mTOR pathway ,Aged ,Cell Proliferation ,Homeodomain Proteins ,Mice, Inbred BALB C ,Cell growth ,Cell migration ,Cell Biology ,Middle Aged ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,A549 Cells ,Apoptosis ,030220 oncology & carcinogenesis ,Cancer research ,Female ,RNA, Long Noncoding ,Carcinogenesis ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
Lung cancer remains the leading cause of cancer-related death all over the world. In spite of the great advances made in surgery and chemotherapy, the prognosis of lung cancer patients is poor. A substantial fraction of long noncoding RNAs (lncRNAs) can regulate various cancers. A recent study has reported that lncRNA HOXB-AS3 plays a critical role in cancers. However, its biological function remains unclear in lung cancer progression. In the current research, we found HOXB-AS3 was obviously elevated in NSCLC tissues and cells. Functional assays showed that inhibition of HOXB-AS3 was able to repress A549 and H1975 cell proliferation, cell colony formation ability and meanwhile, triggered cell apoptosis. Furthermore, the lung cancer cell cycle was mostly blocked in the G1 phase whereas the cell ratio in the S phase was reduced. Also, A549 and H1975 cell migration and invasion capacity were significantly repressed by the loss of HOXB-AS3. The PI3K/AKT pathway has been implicated in the carcinogenesis of multiple cancers. Here, we displayed that inhibition of HOXB-AS3 suppressed lung cancer cell progression via inactivating the PI3K/AKT pathway. Subsequently, in vivo experiments were utilized in our study and it was demonstrated that HOXB-AS3 contributed to lung cancer tumor growth via modulating the PI3K/AKT pathway. Overall, we implied that HOXB-AS3 might provide a new perspective for lung cancer treatment via targeting PI3K/AKT.
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- 2020
9. Long non‐coding RNA F11‐AS1 inhibits HBV‐related hepatocellular carcinoma progression by regulating NR1I3 via binding to microRNA‐211‐5p
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Guidan Xu, Bin Peng, Houji Qin, Meijin Huang, Yibin Deng, Shunqiang Nong, Wujun Wei, and Zhongheng Wei
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Male ,0301 basic medicine ,Receptors, Cytoplasmic and Nuclear ,Apoptosis ,medicine.disease_cause ,Metastasis ,0302 clinical medicine ,Cell Movement ,Viral Regulatory and Accessory Proteins ,Neoplasm Metastasis ,Liver Neoplasms ,hepatocellular carcinoma ,Hep G2 Cells ,nuclear receptor constitutive androstane receptor ,Middle Aged ,Prognosis ,Long non-coding RNA ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,HBx ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Disease Progression ,Molecular Medicine ,Original Article ,Female ,RNA, Long Noncoding ,Protein Binding ,Cell physiology ,Hepatitis B virus ,Carcinoma, Hepatocellular ,Biology ,Models, Biological ,03 medical and health sciences ,microRNA ,medicine ,Humans ,Neoplasm Invasiveness ,Constitutive Androstane Receptor ,Cell Proliferation ,Base Sequence ,Original Articles ,Cell Biology ,medicine.disease ,digestive system diseases ,long non‐coding RNA F11‐antisense 1 ,microRNA‐211‐5p ,MicroRNAs ,030104 developmental biology ,Trans-Activators ,Cancer research - Abstract
Long non‐coding RNAs (lncRNAs) could regulate growth and metastasis of hepatocellular carcinoma (HCC). In this study, we aimed to investigate the mechanism of lncRNA F11‐AS1 in hepatitis B virus (HBV)–related HCC. The relation of lncRNA F11‐AS1 expression in HBV‐related HCC tissues to prognosis was analysed in silico. Stably HBV‐expressing HepG2.2.15 cells were established to explore the regulation of lncRNA F11‐AS1 by HBx protein, as well as to study the effects of overexpressed lncRNA F11‐AS1 on proliferation, migration, invasion and apoptosis in vitro. Subsequently, the underlying interactions and roles of lncRNA F11‐AS1/miR‐211‐5p/NR1I3 axis in HBV‐related HCC were investigated. Additionally, the influence of lncRNA F11‐AS1 and miR‐211‐5p on tumour growth and metastasis capacity of HepG2.2.15 cells were studied on tumour‐bearing nude mice. Poor expression of lncRNA F11‐AS1 was correlated with poor prognosis in patients with HBV‐related HCC, and its down‐regulation was caused by the HBx protein. lncRNA F11‐AS1 was proved to up‐regulate the NR1I3 expression by binding to miR‐211‐5p. Overexpression of lncRNA F11‐AS1 reduced the proliferation, migration and invasion, yet induced apoptosis of HepG2.2.15 cells in vitro, which could be abolished by overexpression of miR‐211‐5p. Additionally, either lncRNA F11‐AS1 overexpression or miR‐211‐5p inhibition attenuated the tumour growth and metastasis capacity of HepG2.2.15 cells in vivo. Collectively, lncRNA F11‐AS1 acted as a modulator of miR‐211‐5p to positively regulate the expression of NR1I3, and the lncRNA F11‐AS1/miR‐211‐5p/NR1I3 axis participated in HBV‐related HCC progression via interference with the cellular physiology of HCC.
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- 2019
10. Isoginkgetin attenuates endoplasmic reticulum stress-induced autophagy of brain after ischemic reperfusion injury
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Yueyong Li, Lingzhang Meng, Baosheng Li, Deyou Huang, Xiaohua Huang, Cheng Lin, Dong Li, Shaocai Qiu, Yingning Wu, Zhongheng Wei, and Xuebin Li
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autophagy ,isoginkgetin ,ischemia/reperfusion (i/r) ,er stress ,TP248.13-248.65 ,Biotechnology - Abstract
Isoginkgetin is characterized by properties of potent anticancer and anti-inflammation. To explore its effect on ischemic stroke, a rat model of ischemia/reperfusion (I/R) injury was established and induced by transient middle cerebral artery occlusion/reperfusion (MCAO/R). Different doses of isoginkgetin were intraperitoneally injected into each rat. Expressions of ER stress activation-related makers including phosphorylated inositol-requiring enzyme 1 (IRE1), phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), activating transcription factor-6 (ATF6), and two autophagy markers (ratio of LC3II/I and Beclin-1) were detected by western blot. Infarct volume, neurological deficits, and brain water content were detected. The results showed that ER stress and autophagy were activated by cerebral (I/R) injury, which could be effectively attenuated following pre-ischemia isoginkgetin administration. Moreover, autophagy induced by ER stress was triggered by the activation of PERK and IRE1 pathways. ER stress inhibitor (4-PBA) and ER related signaling inhibitors including PERK, GSK, IRE1, and DBSA markedly inhibited ER stress and autophagy induced by I/R. In addition, isoginkgetin markedly mitigated cerebral infarction, edema, neuronal apoptosis as well as neurological impairment induced by I/R injury, while tunicamycin (ER stress activator TM) and rapamycin (autophagy activator RAPA) could eliminate these lesions. This research identified a novel therapeutic agent isoginkgetin, which could effectively attenuate I/R injury by blocking autophagy induced by ER stress.
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- 2021
11. Transcriptome Comparison of Brain and Kidney Endothelial Cells in Homeostasis
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Xiaohua Huang, Zhongshi Huang, Zhongheng Wei, Yun Feng, Xuebin Li, Anding Xu, and Chongdong Jian
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Science & Technology ,General Immunology and Microbiology ,Article Subject ,Brain ,Computational Biology ,Epithelial Cells ,General Medicine ,Research & Experimental Medicine ,DEPRESSION ,Kidney ,General Biochemistry, Genetics and Molecular Biology ,Biotechnology & Applied Microbiology ,Medicine, Research & Experimental ,Medicine ,Homeostasis ,Humans ,Transcriptome ,Life Sciences & Biomedicine ,STROKE ,Research Article - Abstract
Endothelial cells are heterogeneous, stemming from multiple organs, but there is still little known about the connection between the brain and kidney endothelial cells, especially in homeostasis. In this study, scRNA-seq results were obtained to compare genetic profiles and biological features of tissue-specific endothelial cells. On this basis, seven endothelial cell subpopulations were identified, two of which were upregulated genes in pathways related to stroke and/or depression, as characterized by neuroinflammation. This study revealed the similarities and distinctions between brain and kidney endothelial cells, providing baseline information needed to fully understand the relationship between renal diseases and neuroinflammation, such as stroke and depression. ispartof: BIOMED RESEARCH INTERNATIONAL vol:2022 ispartof: location:United States status: published
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- 2021
12. A large‐scale transcriptome analysis identified ELANE and PRTN3 as novel methylation prognostic signatures for clear cell renal cell carcinoma
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Bo Wu, Juan Zhang, Li Wang, and Zhongheng Wei
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Male ,0301 basic medicine ,Physiology ,Myeloblastin ,Clinical Biochemistry ,Computational biology ,Biology ,Disease-Free Survival ,Metastasis ,Transcriptome ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,Carcinoma, Renal Cell ,Gene Expression Profiling ,Cancer ,Cell Biology ,Methylation ,DNA Methylation ,Middle Aged ,Prognosis ,medicine.disease ,Gene Expression Regulation, Neoplastic ,Clear cell renal cell carcinoma ,030104 developmental biology ,CpG site ,030220 oncology & carcinogenesis ,DNA methylation ,Female ,Leukocyte Elastase ,Clear cell - Abstract
DNA methylation was involved in the progress of many types of cancer including clear cell renal cell carcinomas (ccRCCs). This study aimed to identify the prognostic DNA methylation biomarkers for the ccRCCs by a large-scale RNA-seq analysis. The DNA methylation data and the corresponding clinical information of the patients with ccRCCs were extracted from TCGA database and randomly divided into the training group and the validation group. The differentially expressed CpG sites and the survival-related CpG sites were further identified, which was combined into CpG sites pair and followed by screening the survival-related pairs. The C-index and the forward search algorithms were constructed to identify the prognostic signatures for the patients with ccRCCs. The prognostic signatures were verified by the validation dataset and the protein-protein interactions (PPI) network analysis was performed on the CPG sites of the signature. A total of 9,861 differentially expressed CPG sites were identified and 567 CpG sites were found to relate to the overall survival (OS) of the patients with ccRCCs. Besides, 1,146 CPG sites pairs were found to be related to the OS of the ccRCCs samples and the signature composed of seven CpG sites pairs were obtained to predict the prognosis of patients with ccRCCs and the results were verified in the validation dataset. Besides, the PPI network analysis showed that ELANE and PRTN3 gene may be associated with the invasion and metastasis of ccRCCs and could function as potential prognostic and therapeutic signatures for ccRCCs.
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- 2019
13. Hes1 Knockdown Exacerbates Ischemic Stroke Following tMCAO by Increasing ER Stress-Dependent Apoptosis via the PERK/eIF2α/ATF4/CHOP Signaling Pathway
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Huatuo Huang, Zhongheng Wei, Huadong Huang, Yingjun Zhang, Yingning Wu, Qifeng Lu, Huangde Fu, Yueyong Li, Pinhu Liao, Houji Qin, and Guizhen Mao
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Male ,0301 basic medicine ,congenital, hereditary, and neonatal diseases and abnormalities ,endocrine system ,Indoles ,Physiology ,Eukaryotic Initiation Factor-2 ,Apoptosis ,Brain damage ,CHOP ,Mice ,eIF-2 Kinase ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Animals ,Gene knockdown ,Cerebral infarction ,business.industry ,Adenine ,General Neuroscience ,ATF4 ,Brain ,Infarction, Middle Cerebral Artery ,General Medicine ,Endoplasmic Reticulum Stress ,medicine.disease ,Activating Transcription Factor 4 ,Mice, Inbred C57BL ,Stroke ,030104 developmental biology ,embryonic structures ,Unfolded protein response ,Cancer research ,Transcription Factor HES-1 ,Original Article ,medicine.symptom ,Signal transduction ,business ,Transcription Factor CHOP ,030217 neurology & neurosurgery ,Signal Transduction - Abstract
Apoptosis induced by endoplasmic reticulum (ER) stress plays a crucial role in mediating brain damage after ischemic stroke. Recently, Hes1 (hairy and enhancer of split 1) has been implicated in the regulation of ER stress, but whether it plays a functional role after ischemic stroke and the underlying mechanism remain unclear. In this study, using a mouse model of ischemic stroke via transient middle cerebral artery occlusion (tMCAO), we found that Hes1 was induced following brain injury, and that siRNA-mediated knockdown of Hes1 increased the cerebral infarction and worsened the neurological outcome, suggesting that Hes1 knockdown exacerbates ischemic stroke. In addition, mechanistically, Hes1 knockdown promoted apoptosis and activated the PERK/eIF2α/ATF4/CHOP signaling pathway after tMCAO. These results suggest that Hes1 knockdown promotes ER stress-induced apoptosis. Furthermore, inhibition of PERK with the specific inhibitor GSK2606414 markedly attenuated the Hes1 knockdown-induced apoptosis and the increased cerebral infarction as well as the worsened neurological outcome following tMCAO, implying that the protection of Hes1 against ischemic stroke is associated with the amelioration of ER stress via modulating the PERK/eIF2α/ATF4/CHOP signaling pathway. Taken together, these results unveil the detrimental role of Hes1 knockdown after ischemic stroke and further relate it to the regulation of ER stress-induced apoptosis, thus highlighting the importance of targeting ER stress in the treatment of ischemic stroke.
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- 2019
14. Genetic variants in IL-33/ST2 pathway with the susceptibility to hepatocellular carcinoma in a Chinese population
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Zhongheng Wei, Zhong-Qiu Tan, Yueyong Li, and Shi-Qing Huang
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Male ,0301 basic medicine ,Oncology ,medicine.medical_specialty ,Carcinoma, Hepatocellular ,Genotype ,Angiogenesis ,Immunology ,medicine.disease_cause ,Polymorphism, Single Nucleotide ,Biochemistry ,Metastasis ,03 medical and health sciences ,0302 clinical medicine ,Asian People ,Gene Frequency ,Internal medicine ,Tumor Microenvironment ,medicine ,Humans ,Immunology and Allergy ,Genetic Predisposition to Disease ,Molecular Biology ,Genotyping ,Alleles ,Genetic Association Studies ,Tumor microenvironment ,business.industry ,Liver Neoplasms ,Interleukin ,Hematology ,Middle Aged ,Interleukin-33 ,medicine.disease ,Interleukin-1 Receptor-Like 1 Protein ,030104 developmental biology ,Case-Control Studies ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Female ,business ,Carcinogenesis ,Signal Transduction - Abstract
Interleukin (IL)-33/ST2 pathway plays a pivotal role in tumorigenesis through influencing cancer stemness, tumor growth, metastasis, angiogenesis, and accumulation of regulatory T cells in tumor microenvironments. The aim of this study was to investigate the association of IL-33 rs7025417 and ST2 rs3821204 with the risk of hepatocellular carcinoma (HCC). Genotyping of IL-33 rs7025417 and ST2 rs3821204 was carried out using a Taqman assay. IL-33 and ST2 mRNA was examined using real-time PCR and plasma IL-33 and sST2 levels were measured using enzyme-linked immunosorbent assay. The ST2 rs3821204 CC genotype was associated with a significantly increased risk of HCC (CC vs. GG: adjusted OR = 2.29, 95% CI, 1.39-3.78; dominant model: adjusted OR = 1.58, 95% CI, 1.12-2.23; recessive model: adjusted OR = 1.88, 95% CI, 1.21-2.93; C vs. G: adjusted OR = 1.53, 95% CI, 1.20-1.95). Gene-environment interaction analysis showed that the risk effect of rs3821204 CG/CC genotypes was more evident in smokers (adjusted OR = 1.70, 95% CI, 1.13-2.55) and drinkers (adjusted OR = 1.57, 95% CI, 1.04-2.37). The increased risk was also observed in combined analysis. Moreover, HCC patients with ST2 rs3821204 CC genotype had higher levels of mRNA and protein expression (P 0.05). These findings suggest that ST2 rs3821204 CC genotype may contribute to hepatocarcinogenesis by enhancing ST2 production at the transcriptional and translational level.
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- 2019
15. Circular RNA hsa_circ_0013958 Functions as an Oncogenic Gene Through Modulating miR-532-3p/WEE1 Axis in Hepatocellular Carcinoma
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Fenqiang Xiao, Yue Ma, Zhongheng Wei, Yongjun Du, Jianchu Wang, Yufu Jun, and Tao Ma
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Cancer Research ,Biology ,medicine.disease_cause ,lcsh:RC254-282 ,Flow cytometry ,In vivo ,medicine ,WEE1 ,Lung cancer ,neoplasms ,Original Research ,medicine.diagnostic_test ,Competing endogenous RNA ,Cell growth ,circ0013958 ,hepatocellular carcinoma ,ceRNA ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,digestive system diseases ,Biomarker (cell) ,Oncology ,Hepatocellular carcinoma ,Cancer research ,miR-532-3p ,Carcinogenesis - Abstract
Backgroundcirc0013958 was identified as a biomarker, which can be used for the diagnosis and screening of lung cancer. However, the role of circ0013958 in hepatocellular carcinoma (HCC) remains unclear.MethodsIn our study, quantitative real-time polymerase chain reaction was performed to determine the levels of circ0013958 in HCC tissues and cell lines. EdU, CCK-8, transwell, flow cytometry and tumorigenesis assays were applied to assess the functions of circ0013958 in HCC in vitro and in vivo. Western blot assay was to detect the expression of WEE1. Luciferase reporter assay, bioinformatics analysis and rescue experiments were used to examine the interaction among circ0013958, miR-532-3p and WEE1.ResultsIt revealed that circ0013958 was significantly up-regulated in HCC, which was positively correlated with poor prognosis of HCC patients. Circ0013958 promoted HCC cell proliferation and invasion, inhibited cell apoptosis in vitro, and promoted tumorigenesis in vivo. Circ0013958 acted as a miR-532-3p sponge to regulate WEE1 expression, thus promoting the progression of HCC.ConclusionsCirc0013958 promotes HCC progression through miR-532-3p/WEE1 axis. Circ0013958 may serve as a potential diagnostic biomarker and therapeutic target of HCC.
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- 2021
16. mRNA expression and DNA methylation analysis of the inhibitory mechanism of H2O2 on the proliferation of A549 cells
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Yepeng, Li, Zhongheng, Wei, Shiqing, Huang, and Bo, Yang
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DNA methylation ,H2O2 ,mRNA expression ,A549 cells ,Articles - Abstract
Reactive oxygen species, particularly hydrogen peroxide (H2O2), can induce proliferation inhibition and death of A549 cells via oxidative stress. Oxidative stress has effect on DNA methylation. Oxidative stress and DNA methylation feature a common denominator: The one carbon cycle. To explore the inhibitory mechanism of H2O2 on the proliferation of lung cancer cells, the present study analysed the mRNA expression and methylation profiles in A549 cells treated with H2O2 for 24 h, as adenocarcinoma is the most common pathological type of lung cancer. The DNA methylation profile was constructed using reduced representation bisulphite sequencing, which identified 29,755 differentially methylated sites (15,365 upregulated and 14,390 downregulated), and 1,575 differentially methylated regions located in the gene promoters were identified using the methylKit. Analysis of the assocaition between gene expression and methylation levels revealed that several genes were downregulated and hypermethylated, including cyclin-dependent kinase inhibitor 3, denticleless E3 ubiquitin protein ligase homolog, centromere protein (CENP)F, kinesin family member (KIF)20A, CENPA, KIF11, PCNA clamp-associated factor and GINS complex subunit 2, which may be involved in the inhibitory process of H2O2 on the proliferation of A549 cells.
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- 2020
17. Co-expressing LRP6 With Anti-CD19 CAR-T Cells for Improved Therapeutic Effect Against B-ALL
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Shan-Shan Yang, Zhongqiu Tan, Cheng-Liang Wan, Ping He, and Zhongheng Wei
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0301 basic medicine ,Cancer Research ,CAR-T cells ,Cell ,lcsh:RC254-282 ,Flow cytometry ,tumor immunotherapy ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,In vivo ,Lactate dehydrogenase ,medicine ,tumor treatment ,B-cell acute lymphocytic leukemia ,Cytotoxicity ,Original Research ,medicine.diagnostic_test ,Chemistry ,Wnt signaling pathway ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Chimeric antigen receptor ,In vitro ,T memory cell ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,030220 oncology & carcinogenesis ,Cancer research ,human activities - Abstract
Background Cellular immunotherapies, such as chimeric antigen receptor modified-T cell (CAR-T) therapy, offers excellent potential for tumor treatment. The memory phenotype of CAR-T has been correlated positively with a therapeutic effect on and prognosis of cancer. Method The proliferation rates of novel CAR-T was determined by cell counting. The phenotypes of CAR-T cells were then detected by flow cytometry. The cell cytotoxicity against tumor cells in vitro was investigated by lactate dehydrogenase assay and luciferase assay. The cytokines secreted during these assays were determined by the cytometric bead array assay. The antitumor ability in vivo was evaluated in NOG mice. Results Co-expression of an LRP6 full-length protein with anti-CD19 CAR significantly improved the memory phenotype of CAR-positive T-cells by enhancing the wnt signaling pathway. As compared with anti-CD19 CAR-T, anti-CD19 CAR-T-LRP6 exhibited more robust cytotoxicity against tumor cells in vitro and in vivo, albeit fewer cytokines were released in vitro. Moreover, the longer survival rate and robust expansion in vivo of anti-CD19 CAR-T-LRP6 cells were found to be effective in inhibiting cancer recurrence. Conclusions CAR co-expressed with LRP6 could sustain the memory phenotype that enabled permanent relief and may further assist in the development of potent and durable T-cell therapeutics.
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- 2020
18. AKR1C1 Contributes to Cervical Cancer Progression via Regulating TWIST1 Expression
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Cheng Lin, Zhongheng Wei, Yueyong Li, Xing Wei, and Zhong-Qiu Tan
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0301 basic medicine ,AKR1C1 ,medicine.medical_treatment ,Uterine Cervical Neoplasms ,Reductase ,Biology ,Biochemistry ,Targeted therapy ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Genetics ,medicine ,Humans ,Molecular Biology ,20-Hydroxysteroid Dehydrogenases ,Ecology, Evolution, Behavior and Systematics ,PI3K/AKT/mTOR pathway ,Cervical cancer ,Aldosterone ,Twist-Related Protein 1 ,Nuclear Proteins ,General Medicine ,medicine.disease ,Human genetics ,In vitro ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Cancer research ,Female ,HeLa Cells - Abstract
Cervical cancer (CC) is a common gynecological malignancy, accounting for 10% of all gynecological cancers. Recently, targeted therapy for CC has shown unprecedented advantages. To improve CC patients' prognosis, there are still urgent needs to develop more promising therapeutic targets. Aldo-keto reductase 1 family member C1 (AKR1C1) is a type of aldosterone reductase and plays a regulatory role in a variety of key metabolic pathways. Several studies indicated that AKR1C1 was highly expressed in a series of tumors, and participated in the progression of these tumors. However, the possible effects of AKR1C1 on CC progression remain unclear. Herein, we revealed AKR1C1 was highly expressed in human CC tissues and correlated with the clinical characteristics of patients with CC. AKR1C1 could regulate the proliferation and invasion of cervical cancer cells in vitro. Further experiments showed that AKR1C1 could regulate TWIST1 expression and AKT pathway. In summary, we confirmed the involvement of AKR1C1 in CC progression, and therefore AKR1C1 may have the potential to be a molecular target for CC treatment.
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- 2020
19. Genes Induced by Panax Notoginseng in a Rodent Model of Ischemia-Reperfusion Injury
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Zechen Wang, Genliang Li, Liuzhi Wei, Xionglin Tang, Qing Huang, Kegong Xie, Chongdong Jian, Jingjie Zhao, Qianli Tang, Jianmin Huang, Xiaohua Huang, Lu Huang, Xuebin Li, Lanqing Meng, Qiuping Chen, Lan Li, Linbo He, Lingzhang Meng, Jihua Wei, Rong Qiu, Dinggui Lu, Jian Chen, Chenyi Zhuo, Qiuju Wei, Qunqiang Luo, Ping Liang, Yang Ouyang, Hongfei Yao, Jun Wu, Anding Xu, Yueyong Li, Linxue Luo, and Zhongheng Wei
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Article Subject ,Biopsy ,medicine.medical_treatment ,Immunology ,Ischemia ,Panax notoginseng ,Rodentia ,Pharmacology ,Neuroprotection ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Immunology and Allergy ,Medicine ,cardiovascular diseases ,KEGG ,Receptor ,Stroke ,030304 developmental biology ,0303 health sciences ,biology ,business.industry ,Gene Expression Profiling ,Computational Biology ,General Medicine ,RC581-607 ,medicine.disease ,biology.organism_classification ,Rats ,Disease Models, Animal ,Gene Ontology ,Gene Expression Regulation ,Reperfusion Injury ,cardiovascular system ,Female ,Immunologic diseases. Allergy ,Transcriptome ,business ,Stroke recovery ,Reperfusion injury ,Biomarkers ,030217 neurology & neurosurgery ,Drugs, Chinese Herbal ,Signal Transduction ,Research Article - Abstract
Stroke is a cerebrovascular disease that results in decreased blood flow. Although Panax notoginseng (PN), a Chinese herbal medicine, has been proven to promote stroke recovery, its molecular mechanism remains unclear. In this study, middle cerebral artery occlusion (MCAO) was induced in rats with thrombi generated by thread and subsequently treated with PN. After that, staining with 2,3,5-triphenyltetrazolium chloride was employed to evaluate the infarcted area, and electron microscopy was used to assess ultrastructural changes of the neurovascular unit. RNA-Seq was performed to determine the differential expressed genes (DEGs) which were then verified by qPCR. In total, 817 DEGs were identified to be related to the therapeutic effect of PN on stroke recovery. Further analysis by Gene Oncology analysis and Kyoto Encyclopedia of Genes and Genomes revealed that most of these genes were involved in the biological function of nerves and blood vessels through the regulation of neuroactive live receptor interactions of PI3K-Akt, Rap1, cAMP, and cGMP-PKG signaling, which included in the 18 pathways identified in our research, of which, 9 were reported firstly that related to PN’s neuroprotective effect. This research sheds light on the potential molecular mechanisms underlying the effects of PN on stroke recovery.
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- 2020
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20. The fluctuating incidence, improved survival of patients with breast cancer, and disparities by age, race, and socioeconomic status by decade, 1981–2010
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Guanming Lu, Jie Li, Shuncong Wang, Jian Pu, Yan-Fei Ma, Haiqing Ma, Zhongheng Wei, Jun Wang, and Huanhuan Sun
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0301 basic medicine ,medicine.medical_specialty ,relative survival rates ,race and socioeconomic status ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,breast cancer ,Epidemiology ,medicine ,Stage (cooking) ,Socioeconomic status ,Original Research ,Relative survival ,business.industry ,Proportional hazards model ,Incidence (epidemiology) ,Cancer ,medicine.disease ,030104 developmental biology ,Oncology ,Cancer Management and Research ,030220 oncology & carcinogenesis ,incidence ,business ,Demography - Abstract
Guanming Lu,1,* Jie Li,2,* Shuncong Wang,3,* Jian Pu,1 Huanhuan Sun,3 Zhongheng Wei,4 Yanfei Ma,1 Jun Wang,5 Haiqing Ma3 1Department of Breast and Thyroid Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China; 2Department of Breast and Thyroid Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, China; 3Department of Oncology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong 519000, China; 4Department of Oncology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China; 5Department of Oncology, General Hospital, Jinan Command of People’s Liberation Army, Jinan, Shandong 250000, China *These authors contributed equally to this work Purpose: Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer-related deaths among women worldwide. However, the data on breast cancer incidence and survival over a long period, especially the dynamic changes in the role of race and socioeconomic status (SES), are scant.Materials and methods: To evaluate treatment outcomes of patients with breast cancer over the past 3 decades, the data from the Surveillance, Epidemiology, and End Results (SEER) registries were used to assess the survival of patients with breast cancer. Period analysis was used to analyze the incidence and survival trend; survival was evaluated by the relative survival rates (RSRs) and Kaplan–Meier analyses. The HRs for age, race, stage, and SES were assessed by Cox regression.Results: A total of 433,366 patients diagnosed with breast cancer between 1981 and 2010 were identified from the original nine SEER registries. The incidences of breast cancer in each decade were 107.1 per 100,000, 117.5 per 100,000, and 109.8 per 100,000. The 10-year RSRs improved each decade, from 70.8% to 81.5% to 85.6% (P
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- 2018
21. Long non‐coding RNA FEZF1‐AS1 promotes breast cancer stemness and tumorigenesis via targeting miR‐30a/Nanog axis
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Yongqiang Li, Liwei Sun, Yixuan Zhang, Zhongheng Wei, Zhi Zhang, and Guanming Lu
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0301 basic medicine ,Homeobox protein NANOG ,Carcinogenesis ,Physiology ,Clinical Biochemistry ,Breast Neoplasms ,Biology ,medicine.disease_cause ,03 medical and health sciences ,0302 clinical medicine ,Breast cancer ,SOX2 ,Cell Movement ,medicine ,Humans ,Neoplasm Invasiveness ,skin and connective tissue diseases ,Cell Proliferation ,Gene knockdown ,CD24 ,CD44 ,CD24 Antigen ,Nanog Homeobox Protein ,Cell Biology ,Prognosis ,medicine.disease ,Long non-coding RNA ,Gene Expression Regulation, Neoplastic ,MicroRNAs ,Hyaluronan Receptors ,030104 developmental biology ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,MCF-7 Cells ,Neoplastic Stem Cells ,Cancer research ,biology.protein ,RNA, Long Noncoding - Abstract
Long non-coding RNAs (lncRNAs) have been verified to modulate the tumorigenesis of breast cancer at multiple levels. In present study, we aim to investigate the role of lncRNA FEZF1-AS1 on breast cancer-stem like cells (BCSC) and the potential regulatory mechanism. In breast cancer tissue, lncRNA FEZF1-AS1 was up-regulated compared with controls and indicated poor prognosis of breast cancer patients. In vitro experiments, FEZF1-AS1 was significantly over-expressed in breast cancer cells, especially in sphere subpopulation compared with parental subpopulation. Loss-of-functional indicated that, in BCSC cells (MDA-MB-231 CSC, MCF-7 CSC), FEZF1-AS1 knockdown reduced the CD44+ /CD24- rate, the mammosphere-forming ability, stem factors (Nanog, Oct4, SOX2), and inhibited the proliferation, migration and invasion. In vivo, FEZF1-AS1 knockdown inhibited the breast cancer cells growth. Bioinformatics analysis tools and series of validation experiments confirmed that FEZF1-AS1 modulated BCSC and Nanog expression through sponging miR-30a, suggesting the regulation of FEZF1-AS1/miR-30a/Nanog. In summary, our study validate the important role of FEZF1-AS1/miR-30a/Nanog in breast cancer stemness and tumorigenesis, providing a novel insight and treatment strategy for breast cancer.
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- 2018
22. FeCeOx catalyzed ultrasonic degradation of diclofenac: Influencing factors, kinetics, and mechanism
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Jie Ye, Shan Chong, Yucan Liu, Panyue Zhang, Guangming Zhang, Ting Huang, Zhongheng Wei, and Nan Zhang
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Diclofenac ,Chemistry ,Kinetics ,medicine ,Degradation (geology) ,Ultrasonic sensor ,Photochemistry ,Mechanism (sociology) ,Catalysis ,medicine.drug - Published
- 2018
23. Sonocatalytic degradation of diclofenac with FeCeOx particles in water
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Guangming Zhang, Yucan Liu, Ting Huang, Zhongheng Wei, Nan Zhang, and Shan Chong
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Acoustics and Ultrasonics ,Singlet oxygen ,Radical ,Sonication ,Organic Chemistry ,chemistry.chemical_element ,02 engineering and technology ,010402 general chemistry ,021001 nanoscience & nanotechnology ,01 natural sciences ,Oxygen ,0104 chemical sciences ,Inorganic Chemistry ,chemistry.chemical_compound ,chemistry ,Desorption ,Chemical Engineering (miscellaneous) ,Environmental Chemistry ,Organic chemistry ,Radiology, Nuclear Medicine and imaging ,Chemical stability ,Leaching (metallurgy) ,0210 nano-technology ,Solid solution ,Nuclear chemistry - Abstract
This paper studies the sonocatalytic degradation of diclofenac in water using FeCeOx-catalyzed ultrasound. The effects of pre-adsorption and gas addition were investigated. Nitrogen adsorption/desorption, SEM, XRD, Raman and XPS analyses of FeCeOx before and after sonication were characterized. The proposed mechanism was based on the microstructure changes of FeCeOx and reactive-species-scavenging performances. The results show that FeCeOx has excellent performance in catalyzing an ultrasonic system in water, and 80% of diclofenac was removed in 30min ([Diclofenac]=20mg/L, FeCeOx amount=0.5g/L, pH=6, ultrasonic density=3.0W/cm3, ultrasonic frequency=20kHz, temperature=298K). The Fe, Ce, and O elements remained highly dispersed in the structure of FeCeOx, and the solid solution structure of FeCeOx remained stable after the reaction. Ce (III) was gradually oxidized to Ce (IV) and Fe (III) was gradually reduced to Fe (II) after the reaction, which indicates that Fe and Ce ions with different valences coexisted in dynamic equilibrium. The amount of oxygen vacancies in FeCeOx significantly decreased after the reaction, which indicates that oxygen vacancy participated in the ultrasonic process. Singlet oxygen 1O2 was the primary reactive species in the degradation process, and the hydroxyl radicals OH and superoxide radical anion O2- also participated in the reaction. FeCeOx had excellent chemical stability with negligible leaching ions in the ultrasonic process.
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- 2017
24. Gene coexpression analysis offers important modules and pathway of human lung adenocarcinomas
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Ying Wang, Zhongheng Wei, Shuxiong Lu, Tan Zhongqiu, Fang Zhang, and Wei Xie
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0301 basic medicine ,Lung Neoplasms ,Physiology ,Clinical Biochemistry ,Adenocarcinoma of Lung ,Computational biology ,Biology ,Collagen Type I ,Extracellular matrix ,Focal adhesion ,03 medical and health sciences ,Phosphatidylinositol 3-Kinases ,0302 clinical medicine ,Interaction network ,Biglycan ,Databases, Genetic ,Cell Adhesion ,Humans ,Gene Regulatory Networks ,Protein Interaction Maps ,Cell adhesion ,Gene ,Focal Adhesions ,Gene Expression Profiling ,Connective Tissue Growth Factor ,Cell Biology ,Extracellular Matrix ,CTGF ,Collagen Type I, alpha 1 Chain ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,Collagen Type III ,030220 oncology & carcinogenesis ,Human genome ,Signal transduction ,Transcriptome ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
Lung adenocarcinomas injured greatly on the people worldwide. Although clinic experiments and gene profiling analyses had been well performed, to our knowledge, systemic coexpression analysis of human genes for this cancer is still limited to date. Here, using the published data GSE75037, we built the coexpression modules of genes by Weighted Gene Co-Expression Network Analysis (WGCNA), and investigated function and protein-protein interaction network of coexpression genes by Database for Annotation, visualization, and Integrated Discovery (DAVID) and String database, respectively. First, 11 coexpression modules were conducted for 5,000 genes in the 83 samples recently. Number of genes for each module ranged from 90 to 1,260, with the mean of 454. Second, interaction relationships of hub-genes between pairwise modules showed great differences, suggesting relatively high scale independence of the modules. Third, functional enrichment of the coexpression modules showed great differences. We found that genes in modules 8 significantly enriched in the biological process and/or pathways of cell adhesion, extracellular matrix (ECM)-receptor interaction, focal adhesion, and PI3K-Akt signaling pathway, and so forth. It was inferred as the key module underlying lung adenocarcinomas. Furthermore, PPI analysis revealed that the genes COL1A1, COL1A2, COL3A1, CTGF, and BGN owned the largest number of adjacency genes, unveiling that they may functioned importantly during the occurrence of lung adenocarcinomas. To summary, genes involved in cell adhesion, ECM-receptor interaction, focal adhesion, and PI3K-Akt signaling pathway play crucial roles in human lung adenocarcinomas.
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- 2019
25. Reflection on the Training of General Medical Students in China from the Development History of General Medicine in Australia and Other Countries*
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Zhongheng Wei, Jian Huang, and Dongling Liang
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Medical education ,Sociology ,China ,Reflection (computer graphics) ,Training (civil) - Published
- 2019
26. Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Zhi-Zhai Luo, Guanming Lu, Yan-Fei Ma, Lifeng Zhao, Jinlan Lu, Qiulan Jiang, Yongcheng Chen, Shi-Qing Huang, Qianfang Huang, Yueyong Li, Qiang Qin, and Zhongheng Wei
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0301 basic medicine ,Homeobox protein NANOG ,Cancer Research ,Carcinogenesis ,Breast Neoplasms ,Biology ,Transfection ,medicine.disease_cause ,lcsh:RC254-282 ,Nanog ,Mice ,03 medical and health sciences ,0302 clinical medicine ,SOX2 ,Transcription (biology) ,Cell Line, Tumor ,LINC00511 ,medicine ,Animals ,Humans ,E2F1 ,Competing endogenous RNA ,Research ,RNA ,Nanog Homeobox Protein ,miR-185-3p ,Middle Aged ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Breast cancer stem cells ,Long non-coding RNA ,MicroRNAs ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,MCF-7 Cells ,Neoplastic Stem Cells ,Cancer research ,Heterografts ,Female ,RNA, Long Noncoding ,E2F1 Transcription Factor - Abstract
Background Emerging evidence have illustrated the vital role of long noncoding RNAs (lncRNAs) long intergenic non-protein coding RNA 00511 (LINC00511) on the human cancer progression and tumorigenesis. However, the role of LINC00511 in breast cancer tumourigenesis is still unknown. This research puts emphasis on the function of LINC00511 on the breast cancer tumourigenesis and stemness, and investigates the in-depth mechanism. Methods The lncRNA and RNA expression were measured using RT-PCR. Protein levels were measured using western blotting analysis. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Sphere-formation assay was also performed for the stemness. Bioinformatic analysis, chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried to confirm the molecular binding. Results LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. Functionally, the gain and loss-of-functional experiments revealed that LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. Mechanically, LINC00511 functioned as competing endogenous RNA (ceRNA) for miR-185-3p to positively recover E2F1 protein. Furthermore, transcription factor E2F1 bind with the promoter region of Nanog gene to promote it transcription. Conclusion In conclusion, our data concludes that LINC00511/miR-185-3p/E2F1/Nanog axis facilitates the breast cancer stemness and tumorigenesis, providing a vital insight for them. Electronic supplementary material The online version of this article (10.1186/s13046-018-0945-6) contains supplementary material, which is available to authorized users.
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- 2018
27. mRNA expression and DNA methylation analysis of the inhibitory mechanism of H2O2 on the proliferation of A549 cells
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Shiqing Huang, Yepeng Li, Bo Yang, and Zhongheng Wei
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0301 basic medicine ,Cancer Research ,CENPA ,biology ,Chemistry ,Bisulfite sequencing ,Promoter ,Methylation ,Molecular biology ,Proliferating cell nuclear antigen ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Differentially methylated regions ,Oncology ,030220 oncology & carcinogenesis ,Gene expression ,DNA methylation ,biology.protein - Abstract
Reactive oxygen species, particularly hydrogen peroxide (H2O2), can induce proliferation inhibition and death of A549 cells via oxidative stress. Oxidative stress has effect on DNA methylation. Oxidative stress and DNA methylation feature a common denominator: The one carbon cycle. To explore the inhibitory mechanism of H2O2 on the proliferation of lung cancer cells, the present study analysed the mRNA expression and methylation profiles in A549 cells treated with H2O2 for 24 h, as adenocarcinoma is the most common pathological type of lung cancer. The DNA methylation profile was constructed using reduced representation bisulphite sequencing, which identified 29,755 differentially methylated sites (15,365 upregulated and 14,390 downregulated), and 1,575 differentially methylated regions located in the gene promoters were identified using the methylKit. Analysis of the assocaition between gene expression and methylation levels revealed that several genes were downregulated and hypermethylated, including cyclin-dependent kinase inhibitor 3, denticleless E3 ubiquitin protein ligase homolog, centromere protein (CENP)F, kinesin family member (KIF)20A, CENPA, KIF11, PCNA clamp-associated factor and GINS complex subunit 2, which may be involved in the inhibitory process of H2O2 on the proliferation of A549 cells.
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- 2020
28. Additional file 2: of Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qin, Qiang, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
- Abstract
Table S2. Primers sequences for ChIP. (DOCX 16Â kb)
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- 2018
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29. Additional file 3: of Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis
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Guanming Lu, Yueyong Li, Yanfei Ma, Jinlan Lu, Yongcheng Chen, Qiulan Jiang, Qin, Qiang, Lifeng Zhao, Qianfang Huang, Zhizhai Luo, Shiqing Huang, and Zhongheng Wei
- Abstract
Table S3. Nanog promoter region. (DOCX 16 kb)
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- 2018
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30. A putative competing endogenous RNA network in cisplatin-resistant lung adenocarcinoma cells identifying potentially rewarding research targets.
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YEPENG LI, SHIQING HUANG, ZHONGHENG WEI, and BO YANG
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NON-small-cell lung carcinoma ,RNA ,NON-coding RNA ,LUNGS ,GENE expression - Abstract
Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer and has a poor 5 year survival rate (<10%). Cisplatin is one of the most effective chemotherapeutic treatments for LUAD, even though it is of limited overall utility due to acquired drug resistance. To identify possible genetic targets for the mitigation of cisplatin resistance, gene expression data from cisplatin-resistant cell lines were integrated with patient information. Expression data for cisplatin-resistant and cisplatin-sensitive A549 cell lines were obtained from the Gene Expression Omnibus database, while LUAD patient data was obtained from The Cancer Genome Atlas (TCGA) database. Differentially expressed mRNAs (DEmRNAs), microRNAs (DEmiRNAs) and long non-coding RNAs (DElncRNAs) were identified between the cisplatin-sensitive and cisplatin-resistant cells. Using the TCGA patient data, 33 DEmRNAs associated with survival were identified. A total of 74 DElncRNAs co-expressed with the survival-associated DEmRNAs, and 11 DEmiRNAs that regulated the survival-associated DEmRNAs, were also identified. A competing endogenous RNA (ceRNA) network was constructed based on the aforementioned results, which included 17 survival-associated DEmRNAs, 9 DEmiRNAs and 16 DElncRNAs. This network revealed 8 ceRNA pathway axes possibly associated with cisplatin resistance in A549 cells. Specifically, the network suggested that the lncRNAs HOXD-AS2, LINC01123 and FIRRE may act as ceRNAs to increase cisplatin resistance in human LUAD cells. Therefore, it was speculated that these lncRNAs represent potentially rewarding research targets. [ABSTRACT FROM AUTHOR]
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- 2020
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31. FeCeOx catalyzed ultrasonic degradation of diclofenac: Influencing factors, kinetics, and mechanism.
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Shan Chong, Guangming Zhang, Panyue Zhang, Nan Zhang, Jie Ye, Ting Huang, Yucan Liu, and Zhongheng Wei
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DICLOFENAC ,ULTRASONICS ,IRON ,CHARGE exchange ,PH effect - Abstract
This paper studied the removal of diclofenac in FeCeO
x catalyzed ultrasonic system. The effects of initial pH, temperature, ultrasonic density and FeCeOx dosage were investigated. Under optimum conditions (pH of 6, temperature of 298 K, ultrasonic density of 2.4 W/cm³, and FeCeOx dosage of 0.7 g/L), more than 80% removal of diclofenac was achieved within 10 min. The kinetic of FeCeOx catalyzed ultrasonic process fitted Behnajady model very well and the reaction rate constant achieved 0.595 min-1 . The dechlorination efficiency was more than 70% and the kinetic of dechlorination followed pseudo-second order model. The reaction mechanism was proposed based on the existence of surface cerium and iron and the abundant oxygen vacancies in the FeCeOx catalyst. Ce(III) and Fe(III) could accept the electrons transferred by oxygen vacancy and the generated ¹O2 could attack diclofenac molecules, resulting in their mineralization to inorganic products. [ABSTRACT FROM AUTHOR]- Published
- 2018
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