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目的:探讨miR-200c调控子宫内膜癌(EC)细胞增殖和侵袭的机制。方法:蛋白印迹和RT-PCR法检测miR-200c、ZEB1和E-cadherin在EC细胞株中的表达。CCK-8检测细胞增殖,Transwell实验检测细胞侵袭力。结果:miR-200c在Ⅱ型EC细胞(HEC-1A和AN3CA)中显著低表达(2.63±0.41和2.83±0.47)。ZEB1在Ⅰ型EC细胞中不表达,而在Ⅱ型EC细胞中高度表达(0.52±0.34和0.81±0.45)。E-cadherin在Ⅰ型EC细胞中高度表达(1.58±0.44和1.01±0.36),而在Ⅱ型EC细胞中极低表达。转染pre-miR-200c后抑制Ⅱ型EC细胞增殖和侵袭能力,A450值分别为1.38±0.27和1.91±0.31,增加AN3CA细胞中E-cadherin的表达。结论:在Ⅱ型EC细胞中miR-200c表达与ZEB1表达呈显著负相关,与E-cadherin表达呈正相关。miR-200c过表达明显抑制Ⅱ型EC细胞增殖和侵袭,miR-200c负性调控ZEB1,参与E-cadherin介导的肿瘤上皮-间质转化。
Objective: To investigate the mechanism of miR-200c regulating the proliferation and invasion of endometrial carcinoma (EC) cells. Methods: Western blotting and RT-PCR were used to detect the expression of miR-200c, ZEB1 and E-cadherin in EC cell lines. Cell proliferation was detected by CCK-8, and cell invasiveness was detected by Transwell assay. Results: miR-200c was significantly down-regulated in type II EC cells (HEC-1A and AN3CA) (2.63 ± 0.41 and 2.83 ± 0.47). ZEB1 was not expressed in type I EC cells but highly expressed in type II EC cells (0.52 ± 0.34 and 0.81 ± 0.45). E-cadherin was highly expressed in type I EC cells (1.58 ± 0.44 and 1.01 ± 0.36), while it was extremely low in type II EC cells. After transfected with pre-miR-200c, the proliferation and invasion ability of type II EC cells were inhibited. The A450 values were 1.38 ± 0.27 and 1.91 ± 0.31, respectively, which increased the expression of E-cadherin in AN3CA cells. CONCLUSION: There is a significant negative correlation between the expression of miR-200c and the expression of ZEB1 in type II EC cells, which is positively correlated with the expression of E-cadherin. miR-200c overexpression significantly inhibited the proliferation and invasion of type II EC cells, and miR-200c negatively regulated ZEB1, which was involved in E-cadherin-mediated tumor epithelial-mesenchymal transition.