Xizhong Shen

Fudan University, Shanghai, Shanghai Shi, China

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Publications (52)170.29 Total impact

  • Yi Wang · Taotao Liu · Wenqing Tang · Bin Deng · Yanjie Chen · Jimin Zhu · Xizhong Shen

    No preview · Article · Jan 2016 · Cellular Physiology and Biochemistry
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    ABSTRACT: Background and objective: Inhibitors of apoptosis proteins (IAPs) have been well investigated in human cancers, where they are frequently overexpressed and associated with poor prognosis. Here we explored the role of baculoviral IAP repeat containing 6 (BIRC6), a member of IAPs, in human colorectal cancer (CRC). Methods: We used Western blotting and immunohistochemistry to examine BIRC6 expression in 7 CRC cell lines and 126 CRC clinical samples. We determined the biological significance of BIRC6 in CRC cell lines by a lentivirus-mediated silencing method. Results: We reported that BIRC6 was overexpressed in CRC cell lines and clinical CRC tissues. BIRC6 overexpression was correlated with tumor size and invasion depth of CRC. BIRC6 overexpression is associated with worse overall survival (OS) (P = 0.001) and shorter disease-free survival (DFS) (P = 0.010). BIRC6 knockdown inhibited cell proliferation, arrested cell cycle at S phase, downregulated cyclin A2, B1, D1 and E1 levels, and sensitized CRC cells to chemotherapy in vitro and in vivo. Conclusions: Taken together, these data suggests that BIRC6 overexpression is a predictor of poor prognosis in colorectal cancer and BIRC6 could be a potential target of CRC therapy.
    Preview · Article · May 2015 · PLoS ONE
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    ABSTRACT: The genes that encode inhibitor of apoptosis proteins (IAPs) are frequently overexpressed in human cancers. However, the expression pattern and clinical significance of BIRC6, a member of IAPs, in hepatocellular carcinoma (HCC) remains unclear. Here we investigated the role of BIRC6 in hepatocellular carcinogenesis. We used immunoblot and immunochemical analyses to determine the levels of BIRC6 in 7 hepatoma cell lines and 160 HCC specimens. We evaluated the proognostic value of BIRC6 expression and its association with clinical parameters. A lentivirus-mediated silencing method was used to knockdown BIRC6, and the biological consequences of BIRC6 silencing in three hepatoma cell lines were investigated in vitro and in vivo. We found that BIRC6 overexpression was significantly correlated with serum ALT level and HCC vascular invasion. Patients with positive BIRC6 expression in tumor tissue had a poor survival and a high rate of recurrence. BIRC6 knockdown remarkably suppressed cell proliferation, caused G1/S arrest and sensitized hepatoma cells to sorafenib-induced apoptosis in hepatoma cells, which was partly reversed by RNA interference targeting p53. The mechanistic study revealed that BIRC6 interacted with p53 and facilitated its degradation. The in vivo study showed that BIRC6 knockdown inhibited xenograft tumor growth and increased the sensitivity of tumor cells to sorafenib in nude mice. Taken together, these findings demonstate that BIRC6 overexpression in HCC specimens is indicative of poor prognosis and that its interaction with p53 facilitates the degradation of p53, leading to carcinogenesis and an anti-apoptotic status. © 2014 Wiley Periodicals, Inc.
    Full-text · Article · Sep 2014 · International Journal of Cancer
  • Danying Zhang · Shuqiang Weng · Ling Dong · Xizhong Shen

    No preview · Article · Sep 2014 · Journal of Digestive Diseases
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    ABSTRACT: Patients with esophageal squamous cell carcinoma (ESCC) are often diagnosed with advanced diseases that respond poorly to chemotherapy. Here we reported that Apollon, a membrane-associated inhibitor of apoptosis protein, was overexpressed in ESCC cell lines and clinical ESCC tissues, and Apollon overexpression clinically correlated with poor response to chemotherapy (P = 0.001), and short overall survival (P = 0.021). Apollon knockdown increased cisplatin/docetaxel-induced apoptosis, mitochondrial dysfunction and cytochrome c release in two ESCC cell lines. Apollon knockdown potentiated cisplatin/docetaxel-induced long-term cell growth inhibition, and enhanced chemosensitivity of ESCC cells to cisplatin/docetaxel in xenograft tumor models. Apollon knockdown also enhanced cisplatin/docetaxel-induced activation of caspase-8 (extrinsic pathway) and caspase-9 (intrinsic pathway) in ESCC cells and xenograft tumor models. Mechanism studies revealed that the effect of Apollon on chemosensitivity is mainly mediated by Smac. Apollon expression strongly and negatively correlated with Smac expression in clinical ESCC tissues (P = 0.001). Apollon targeted Smac for degradation in ESCC cells. The effect of Apollon on chemosensitivity was reversed by Smac knockdown in ESCC cells. Taken together, our data show association of Apollon expression with chemotherapeutic response in ESCC, and provide a strong rationale for combining Apollon antagonism with chemotherapy to treat ESCC.
    Full-text · Article · Aug 2014 · Oncotarget
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    ABSTRACT: The clinical data of a patient with acute-on-chronic liver failure were analyzed retrospectively. The patient has suffered from hepatitis B for 30 years. His liver function deteriorated, yielding Child-Pugh grade C and reaching a model for end-stage liver disease score of 33 points within a short period; this condition was complicated with highly active variceal bleeding and coagulation system failure (PT > 100 s). The patient also presented hepatocellular carcinoma. Comprehensive treatments included effective inhibition of hepatitis B virus replication and intensive care support. Piggyback orthotopic liver transplantation was performed as the final treatment. The patient recovered uneventfully and was discharged after surgery.
    No preview · Article · May 2014 · Frontiers of Medicine
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    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases, and the pathogenesis is still not well known. The farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily and plays an essential role in maintaining bile acid and lipid homeostasis. In this study, we study the role of FXR in the pathogenesis of NFALD. We found that FXR deficient (FXR(-/-)) mice fed methionine- and choline-deficient (MCD) diet had higher serum ALT and AST activities and lower hepatic triglyceride levels than wild-type (WT) mice fed MCD diet. Expression of genes involved in inflammation (VCAM-1) and fibrosis (α-SMA) was increased in FXR(-/-) mice fed MCD diet (FXR(-/-)/MCD) compared to WT mice fed MCD diet (WT/MCD). Although MCD diet significantly induced hepatic fibrosis in terms of liver histology, FXR(-/-)/MCD mice showed less degree of hepatic steatosis than WT/MCD mice. Moreover, FXR deficiency synergistically potentiated the elevation effects of MCD diet on serum and hepatic bile acids levels. The super-physiological concentrations of hepatic bile acids in FXR(-/-)/MCD mice inhibited the expression of genes involved in fatty acid uptake and triglyceride accumulation, which may be an explanation for less steatosis in FXR(-/-)/MCD mice in contrast to WT/MCD mice. These results suggest that hepatic bile acids accumulation could override simple steatosis in hepatic injury during the progression of NAFLD and further emphasis the role of FXR in maintaining hepatic bile acids homeostasis in liver disorders and in hepatic protection.
    No preview · Article · Apr 2014 · Biochemical and Biophysical Research Communications
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    Guangxi Zhao · Jing Li · Jiyao Wang · Xizhong Shen · Jianyong Sun
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    ABSTRACT: Aquaporins (AQPs) plays an important role in transcellular water movement, but the AQPs expression profile has not been demonstrated in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis which closely mimics human Crohn's disease (CD) histopathologically. To solve the problem, 30 female Sprague-Dawley (SD) rats were randomly divided into a model group (n=18), an ethanol control group (n=6) and a normal control group (n=6). On day 1, the rats in the model group received TNBS+50% ethanol via the rectum, while the ethanol control rats received an equal volume of 50% ethanol and the normal control rats did not receive any treatment. All rats were sacrificed on day 7, and ileum, proximal colon and distal colon specimens were obtained to examine the alteration in AQP3 and AQP8 using real-time polymerase chain reaction, Western blot analysis and immunohistochemistry. As a result, exposure to TNBS+ethanol resulted in a marked decrease in both the mRNA and protein expression of AQP3 and AQP8, with the exception of AQP8 protein which was negative in the distal colon in all three groups. These reductions in AQP3 and AQP8 were accompanied by an increase in intestinal inflammation and injury. The results obtained here implied that both AQP3 and AQP8 may be involved in the pathogenesis of inflammatory bowel disease.
    Preview · Article · Nov 2013 · Biochemical and Biophysical Research Communications
  • Tiancheng Luo · Shengdi Wu · Xizhong Shen · Lei Li
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    ABSTRACT: Colorectal cancer (CRC) is a major cause of morbidity and mortality throughout the world. However, the genetic alterations and molecular mechanism of the early onset CRCs are not fully investigated. The present study aimed to characterize early onset CRC by analyzing its gene expression compared with normal controls and to identify network-based biomarkers of early onset CRC. The gene expression profiles of early onset CRC were downloaded from Gene Expression Omnibus and the differentially expressed genes (DEGs) in CRC patients were identified. Then, a protein-protein interaction (PPI) network was constructed and the clusters in PPI were analyzed by ClusterONE. Furthermore, the gene ontology functional analysis and pathway enrichment analysis were conducted to the modules in PPI network. A systems biology approach integrating microarray data and PPI was further applied to construct a PPI network in CRC. Total 631 DEGs were identified from the early onset CRC compared to healthy controls. These genes were found to be involved in several biological processes, including cell communication, cell proliferation, cell shape and apoptosis. Five functional modules which may play important roles in the initiation of early onset CRC were identified from the PPI network. Functional annotation revealed that these five modules were involved in the pathways of signal transduction, carcinogenesis and metastasis. The hub nodes of these five modules, CDC42, TEX11, QKI, CAV1 and FN1, may serve as the biomarkers of early onset CRC and have the potential to be targets for therapeutic intervention. However, further investigations are still needed to confirm our findings.
    No preview · Article · Nov 2013 · Molecular Biology Reports
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    Yingnan Huang · Hao Wu · Ruyi Xue · Taotao Liu · Ling Dong · Jun Yao · Yang Zhang · Xizhong Shen
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    ABSTRACT: This study is to explore the different expressions of serum N-glycoproteins and glycosylation sites between hepatocellular carcinoma (HCC) patients and healthy controls. We combined high abundant proteins depletion and hydrophilic affinity method to enrich the glycoproteins. Through liquid chromatography-tandem mass spectrometry (LC-MS/MS), we extensively surveyed different expressions of glycosylation sites and glycoproteins between the two groups. This approach identified 152 glycosylation sites and 54 glycoproteins expressed differently between HCC patients and healthy controls. With the absolute values of Pearson coefficients of at least 0.8, eight proteins were identified significantly up or down regulated in HCC serum. Those proteins are supposed to be involved in several biological processes, cellular components and molecular functions of hepatocarcinogenesis. Several of them had been reported abnormally regulated in several kinds of malignant tumors, and may be promising biomarkers of HCC. Our work provides a systematic and quantitative method of glycoproteomics and demonstrates some key changes in clinical HCC serum. These proteomic signatures may help to unveil the underlying mechanisms of hepatocarcinogenesis and may be useful for the exploration of candidate biomarkers.
    Full-text · Article · Oct 2013 · PLoS ONE
  • Qunyan Yao · Yizheng Lin · Xi Li · Xizhong Shen · Jiyao Wang · Chuantao Tu
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    ABSTRACT: Neoangiogenesis and the development of an abnormal angio-architecture in the liver are strongly linked with progressive fibrogenesis. This study aimed to evaluate the ability of curcumin to protect liver fibrosis-associated angiogenesis and capillarization of the sinusoids in experimental rats. Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl4) with or without curcumin for 6 weeks. The results suggest that curcumin treatment markedly attenuated CCl4-induced liver fibrosis, as assessed by histology and hydroxyproline content, and inhibited hepatic stellate cell activation. Curcumin ameliorated hepatic angiogenesis, as assessed by measuring microvessel density using Von Willebrand factor staining and by examining the expression of the endothelial cell markers CD31 and vascular endothelial growth factor receptor (VEGFR)-2 in the livers. Pathologic remodeling of liver sinusoidal capillarization, as assessed by electron-microscopic analysis of Disse's space and by evaluation of the levels of basement membrane protein expression, was also attenuated by curcumin administration. The intrahepatic gene or protein expression of hypoxia-inducible factor-1α, VEGFR-1, placental growth factor, and cyclooxygenase-2 decreased with treatment with curcumin in fibrotic rats. In conclusion, curcumin ameliorates hepatic angiogenesis and sinusoidal capillarization in CCl4-induced rat liver fibrosis through suppressing multiple pro-angiogenic factors.
    No preview · Article · Jul 2013 · Toxicology Letters
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    ABSTRACT: Our previous studies showed that cell surface β 1,4-galactosyltransferase 1 (β1,4GT1) negatively regulated cell survival through inhibition and modulation of the epidermal growth factor receptor (EGFR) signaling pathway in human hepatocellular carcinoma (HCC) SMMC-7721 cells. However, the underlying mechanism remains unclear. Here we demonstrated that β 1,4-galactosyltransferase 1 (β1,4GT1) interacted with EGFR in vitro by GST pull-down analysis. Furthermore, we demonstrated that β1,4GT1 bound to EGFR in vivo by co-immunoprecipitation and determined the co-localization of β1,4GT1 and EGFR on the cell surface via confocal laser scanning microscopy analysis. Finally, using (125)I-EGF binding experiments and Western blot analysis, we found that overexpression of β1,4GT1 inhibited (125)I-EGF binding to EGFR, and consequently reduced the levels of EGFR dimerization and phosphorylation. In contrast, RNAi-mediated knockdown of β1,4GT1 increased the levels of EGFR dimerization and phosphorylation. These data suggest that cell surface β1,4GT1 interacts with EGFR and inhibits EGFR activation.
    Preview · Article · Apr 2013 · Biochemical and Biophysical Research Communications
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    ABSTRACT: We report a highly sensitive competitive-type assay for multiplexing electrochemical detection of clenbuterol in pig urine using a 16-sensor array. In this design, the clenbuterol was first conjugated with bovine serum albumin (BSA), and then the conjugates were immobilized on the electrode surface to compete with the free clenbuterol in the sample for specific antibody. Under the optimal conditions, the reproducibility of the clenbuterol electrochemical immunosensor was evaluated to be 3.4 % (coefficient of variation, CV) and the limit of detection was estimated to be 1.3 pg/mL. The very low detection limit was probably derived from the higher efficiency of the competitive immunoreaction caused by appropriate quantities of the clenbuterol immobilized on the 16-sensor array and the suitable amount of anti-clenbuterol antibody in the assay system.
    No preview · Article · Apr 2013 · Electroanalysis
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    ABSTRACT: BACKGROUNDAIM: To investigate the roles of biomedical factors, hepatitis B virus (HBV) DNA levels, genotypes, and specific viral mutation patterns on the progression of hepatocellular carcinoma (HCC) patients below 40 years of age in Qidong, China. We conducted a case-control study within a cohort of 2387 male HBV carriers who were recruited from August, 1996. The HBV DNA sequence was determined in 49 HCC and 90 chronic hepatitis (CH) patients below 40 years of age. Mutation exchanges during follow-up in 32 cases were compared with 65 controls with paired serum samples. In addition, a consecutive series of samples from 14 HCC cases were employed to compare the sequences before and after the occurrence of HCC. After adjustment for age, history of cigarette smoking and alcohol consumption, HBeAg positive, HBV DNA levels ≥4.00 log10 copies/mL, pre-S deletion, T1762/A1764 double mutations, and T1766 and/or A1768 mutations were associated with risk of young age HCC. Moreover, the presence of an increasing number of HCC-related mutations (pre-S deletion, T1762/A1764, and T1766 and/or A1768 mutations) was associated with an increased risk of young age HCC. Paired samples analysis indicated that the increased HCC risk for at-risk sequence mutations were attributable to the persistence of these mutations, but not a single time point mutation. The longitudinal observation demonstrated a gradual combination of pre-S deletion, T1762/A1764 double mutations, and T1766 and/or A1768 mutations during the development of HCC. High HBV DNA levels and pre-S deletion were independent risk factors of young age HCC. Combination of pre-S deletion and core promoter mutations increased the risk and persistence of at-risk sequence mutations is critical for HCC development.
    Preview · Article · Mar 2013 · PLoS ONE
  • Yi Wang · Bin Deng · Wenqing Tang · Taotao Liu · Xizhong Shen
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    ABSTRACT: Aim: The purpose of this study was to explore the mechanisms of TGF-β1 mediated immunosuppression in tumor stroma. Methods: The expression of TGF-β1 was investigated in Huh7, Hep 3B, SGC-7901, Eca-109 and Hepa1-6 cell lines using immunofluorescence. Knocked-down TGF-β1 of the Hepa1-6 cell line was established through lentivirus-based RNA interference. The interference efficiency of the TGF-β1 gene was tested by real-time PCR and ELISA; the expression of Foxp3, IFN-γ and CD83 in CD4(+), CD8(+) or dendritic cells was examined via flow cytometry; and the tumorigenic ability of the cancer cells was investigated in the animal experiments. Results: The diverse digestive cancer cells were found to secrete TGF-β1, mRNA of which was knocked down by 78 % thanks to lentivirus-based interference in Hepa1-6 cells. Flow cytometry showed that CD4(+)CD25(+)Foxp3(+) regulatory T cells significantly increased in hepatocellular carcinoma patients when compared with those in the healthy controls. The supernatant from Hepa1-6 cells and recombinant TGF-β1 significantly induced the expression of Foxp3 gene in vitro, while that from sh TGF-β1 Hepa1-6 cells restored it. Hepa1-6 cells inhibited IFN-γ and CD83 expression in CD8(+) or dendritic cells by secreting TGF-β1. The animal experiments indicated that the knockdown TGF-β1 gene impaired the tumorigenic ability of Hepa1-6 cells. Conclusion: TGF-β1, expressed in cancer cells, might be a potential therapeutic target for cancer treatment.
    No preview · Article · Jan 2013 · Digestive Diseases and Sciences
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    ABSTRACT: Ubiquitin C-terminal hydrolase 37 (UCH37) plays a crucial role in numerous biological processes and is also involved in oncogenesis. In this study, clinicopathologic data showed that UCH37 was over-expressed in hepatocellular carcinoma (HCC) cancerous tissues and was a significant predictor for time to recurrence (TTR). In vitro, we discovered that UCH37 could promote cell migration and invasion. Subsequently, we utilized Isobaric Tags for Relative and Absolute Quantitation (iTRAQ) to identify differentially expressed proteins in UCH37 over-expressing cells compared with the control cells, and found that PRP19, an essential RNA splicing factor, was up-regulated. The relationship between UCH37, PRP19 and the capability of cell migration and invasion was further confirmed. Collectively, this study demonstrated that UCH37 could promote cell migration and invasion in HCC cell lines through interacting and deubiquitinating PRP19, and suggested that UCH37 could be a novel predictor for HCC recurrence after curative resection.
    Preview · Article · Dec 2012 · Biochimica et Biophysica Acta
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    Kang Song · Jiayong Yi · Xizhong Shen · Yu Cai
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    ABSTRACT: Background A number of case-control studies were conducted to investigate the association of glutathione S-transferase (GST) genetic polymorphisms and hepatocellular carcinoma (HCC) risk. However, these studies have yielded contradictory results. We therefore performed a meta-analysis to derive a more precise estimation of the association between polymorphisms on GSTM1, GSTT1 and HCC. Methodology/Prinicpal Findings PubMed, EMBASE, ISI web of science and the CNKI databases were systematically searched to identify relevant studies. Data were abstracted independently by two reviewers. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to assess the strength of association. Potential sources of heterogeneity were also assessed by subgroup analysis and meta-regression. Funnel plots and Egger’s linear regression were used to test publication bias among the articles. A total of 34 studies including 4,463 cases and 6,857 controls were included in this meta-analysis. In a combined analysis, significantly increased HCC risks were found for null genotype of GSTM1 (OR = 1.29, 95% CI: 1.06–1.58; P = 0.01) and GSTT1 (OR = 1.43, 95% CI: 1.22–1.68; P<10−5). Potential sources of heterogeneity were explored by subgroup analysis and meta-regression. Significant results were found in East Asians and Indians when stratified by ethnicity; whereas no significant associations were found among Caucasians and African populations. By pooling data from 12 studies that considered combinations of GSTT1 and GSTM1 null genotypes, a statistically significant increased risk for HCC (OR = 1.88, 95% CI: 1.41–2.50; P<10−4) was detected for individuals with combined deletion mutations in both genes compared with positive genotypes. Conclusions/Significance This meta-analysis suggests that the GSTM1 and GSTT1 null genotype may slightly increase the risk of HCC and that interaction between unfavourable GSTs genotypes may exist.
    Preview · Article · Nov 2012 · PLoS ONE
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    Yanli Wen · Hao Pei · Ye Shen · Junjie Xi · Meihua Lin · Na Lu · Xizhong Shen · Jiong Li · Chunhai Fan
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    ABSTRACT: Supporting Information
    Preview · Dataset · Nov 2012
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    Yanli Wen · Hao Pei · Ye Shen · Junjie Xi · Meihua Lin · Na Lu · Xizhong Shen · Jiong Li · Chunhai Fan
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    ABSTRACT: MicroRNAs (miRNAs) have been identified as promising cancer biomarkers due to their stable presence in serum. As an alternative to PCR-based homogenous assays, surface-based electrochemical biosensors offer great opportunities for low-cost, point-of-care tests (POCTs) of disease-associated miRNAs. Nevertheless, the sensitivity of miRNA sensors is often limited by mass transport and crowding effects at the water-electrode interface. To address such challenges, we herein report a DNA nanostructure-based interfacial engineering approach to enhance binding recognition at the gold electrode surface and drastically improve the detection sensitivity. By employing this novel strategy, we can directly detect as few as attomolar (<1, 000 copies) miRNAs with high single-base discrimination ability. Given that this ultrasensitive electrochemical miRNA sensor (EMRS) is highly reproducible and essentially free of prior target labeling and PCR amplification, we also demonstrate its application by analyzing miRNA expression levels in clinical samples from esophageal squamous cell carcinoma (ESCC) patients.
    Full-text · Article · Nov 2012 · Scientific Reports
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    Qiman Sun · Kang Song · Xizhong Shen · Yu Cai
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    ABSTRACT: KCNQ1 (potassium voltage-gated channel KQT-like sub-family, member 1) encodes a pore-forming subunit of a voltage-gated K(+) channel (KvLQT1) that plays a key role for the repolarization of the cardiac action potential as well as water and salt transport in epithelial tissues. Recently, genome-wide association studies have identified KCNQ1 as a type 2 diabetes (T2D) susceptibility gene in populations of Asian descent. After that, a number of studies reported that the rs2237892 and rs2237895 polymorphism in KCNQ1 has been implicated in T2D risk. However, studies on the association between these polymorphism and T2D remain conflicting. To investigate this inconsistency, we performed this meta-analysis. Databases including Pubmed, EMBASE, Web of Science and China National Knowledge Infrastructure (CNKI) were searched to find relevant studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. Potential sources of heterogeneity were also assessed by subgroup analysis and meta-regression. A total of 25 articles involving 70,577 T2D cases and 99,068 controls were included. Overall, the summary odds ratio of C allele for T2D was 1.32 (95% CI 1.26-1.38; P<10-5) and 1.24 (95% CI: 1.20-1.29; P<10-5) for KCNQ1 rs2237892 and rs2237895 polymorphisms, respectively. Significant results were also observed using co-dominant, dominant and recessive genetic models. After stratifying by ethnicity, sample size, and diagnostic criteria, significant associations were also obtained. This meta-analysis suggests that the rs2237892 and rs2237895 polymorphisms in KCNQ1 are associated with elevated type 2 diabetes susceptibility.
    Preview · Article · Nov 2012 · PLoS ONE

Publication Stats

1k Citations
170.29 Total Impact Points

Institutions

  • 2005-2015
    • Fudan University
      • • Department of Biochemistry and Molecular Biology
      • • Department of Chemistry
      • • Department of Macromolecular Science
      Shanghai, Shanghai Shi, China
  • 2012
    • Zhongshan University
      Shanghai, Shanghai Shi, China