miR-200 family expression is downregulated upon neoplastic progression of Barrett's esophagus
miR-200 family expression is downregulated upon neoplastic progression of Barrett's esophagus作者机构:Department of Surgery Flinders University Bedford Park Department of Gastroenterology and Hepatology Flinders University Bedford Park Department of Surgery Erasmus Medical Centre
出 版 物:《World Journal of Gastroenterology》 (世界胃肠病学杂志(英文版))
年 卷 期:2011年第17卷第8期
页 面:1036-1044页
核心收录:
学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金:Supported by National Health and Medical Research Council Australia
主 题:miRNA Barrett’s esophagus Esophageal adenocarcinoma miR-200 Epithelial to mesenchymal transition Apoptosis Proliferation Epithelium
摘 要:AIM: To investigate miR-200 family expression in Barrett s epithelium, gastric and duodenal epithelia, and esophageal adenocarcinoma. METHODS: Real-time reverse transcriptase-polymerase chain reaction was used to measure miR-200, ZEB1 and ZEB2 expression. Ingenuity Pathway Analysis of miR-200 targets was used to predict biological outcomes. RESULTS: Barrett s epithelium expressed lower levels of miR-141 and miR-200c than did gastric and duodenal epithelia (P 0.001). In silico analysis indicated roles for the miR-200 family in molecular pathways that distinguish Barrett s epithelium from gastric and duodenalepithelia, and which control apoptosis and proliferation. All miR-200 members were downregulated in adenocarcinoma (P 0.02), and miR-200c expression was also downregulated in non-invasive epithelium adjacent to adenocarcinoma (P 0.02). The expression of all miR-200 members was lower in Barrett s epithelium derived high-grade dysplastic cell lines than in a cell line derived from benign Barrett s epithelium. We observed signif icant inverse correlations between miR-200 family expression and ZEB1 and ZEB2 expression in Barrett s epithelium and esophageal adenocarcinoma (P 0.05). CONCLUSION: miR-200 expression might contribute to the anti-apoptotic and proliferative phenotype of Barrett s epithelium and regulate key neoplastic processes in this epithelium.