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

作　　者：刘娜[1] 曾洁[1] 张小媚[1] 杨琼[1] 廖迪[1] 陈高文[1] 王沂峰[1] 

机构地区：[1]南方医科大学珠江医院妇产科,广州510282

出　　处：《广东医学》2014年第21期3294-3298,共5页Guangdong Medical Journal

基　　金：广东省教育厅科技创新项目(编号:2013KJCX0042);南方医科大学珠江医院人才引进基金项目

摘　　要：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.

关 键 词：卵巢癌 微小RNA 转移 上皮间质转化 

分 类 号：R737.31[医药卫生—肿瘤]