Expression of miRNA in human epithelial ovarian cancer

发现miR-34 b具有启动子高甲基化，当逆转时，在用5-氮杂-2 '脱氧胞苷处理的子宫内膜浆液性癌（ESC）细胞系中恢复miR-34 b表达。miR-34 b转染抑制ESC细胞生长、迁移和最显著的侵袭。这些作用由miR-34 b靶基因间充质上皮转化因子（MET）介导。在ESC细胞系中，随着miR-34 b的恢复，MET的表达降低。总之，我们的数据表明，miR-34 b在子宫内膜癌的分子发病机制中发挥作用。

miR-34b was found to have promoter hypermethylation, which when reversed, restored miR-34b expression in the endometrial serous cancer (ESC)cell lines treated with 5-aza-2' deoxycytidine. miR-34b transfection inhibited ESC cell growth, migration and most notably invasion. These effects were mediated by miR-34b target gene, the mesenchymal epithelial transition factor (MET). The expression of MET was reduced following the restoration of miR-34b in ESC cell lines. In summary, our data suggest that miR-34b plays a role in the molecular pathogenesis of endometrial cancer.