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.
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.
基金
Supported by National Health and Medical Research Council, Australia
