miR-200a靶向上皮间质转化对卵巢癌细胞黏附与迁移能力的影响

miR- 200a targeted epithelial- mesenchymal transition effect on adhesion and migration ability of ovarian cancer cell

目的探讨miR-200a对卵巢癌细胞转移的调控作用及其机制。方法利用慢病毒表达载体,在卵巢癌细胞株SK-OV-3和OVCAR-3中构建稳定上调miR-200a的卵巢癌细胞模型;采用细胞黏附实验和Transwell实验,分别检测miR-200a对卵巢癌细胞黏附和迁移能力的调控作用;利用蛋白印迹(Western blot)实验检测miR-200a对上皮间质转化(EMT)相关基因表达水平的调控作用。结果成功构建了稳定上调miR-200a的卵巢癌细胞模型SK-OV-3和OVCAR-3;miR-200a过表达抑制了SK-OV-3和OVCAR-3卵巢癌细胞的黏附和迁移能力,上调了上皮细胞表型相关E-钙黏蛋白的表达,降调了间质细胞表型相关波形蛋白和纤连蛋白的表达。结论 miR-200a可能通过阻碍EMT抑制了卵巢癌细胞的转移。

Objective To investigate the effects and mechanisms of miR -200a regulation on ovarian cancer me- tastasis. Methods Over - expression of miR - 200a was induced in ovarian cancer cell lines SK - OV - 3 and OVCAR - 3 by lentiviral vector. The cell adhesion assay and transwell experiments were used to detect the adhesion and migration of ovarian cancer cells. Epithelial- mesenchymal transition （EMT） -related gene expression regulated by miR- 200a was validated by Western blot. Results The miR - 200a over - expression ovarian cancer cell SK - OV - 3 and OVCAR - 3 was successfully constructed. The over - expression of miR - 200a inhibited the abilities of adhesion and migration in SK - OV - 3 and OVCAR - 3 cells, up - regulated epithelial cell marker associated E - cadherin, and down - regulated mesenchymal cell marker associated vimentin and fibronectin. Conclusion miR - 200a may inhibit ovarian cancer metas- tasis by blocking EMT.