Long noncoding RNA H19 promotes transforming growth factor-β-induced epithelial–mesenchymal transition by acting as a competing endogenous RNA of miR-370-3p in ovarian cancer cells

Abstract

Ovarian cancer is a gynecological malignant tumor with a high mortality rate among women, owing to metastatic progression and recurrence. Acquisition of invasiveness is accompa­nied by the loss of epithelial features and a gain of a mesenchymal phenotype, a process known as epithelial–mesenchymal transition (EMT). Transforming growth factor-β (TGF-β) has been implicated in the regulation of EMT. In the present study, we aimed to investigate the role of long noncoding RNA H19 and microRNA-370 (miR-370-3p) in TGF-β-induced EMT. Ovarian cancer cell lines SKOV-3 and OVCAR3 were incubated with different concentrations of TGF-β, and the results showed that TGF-β treatment upregulated H19 and downregulated miR-370-3p. In addition, an H19 knockdown or miR-370-3p overexpression suppressed TGF-β-induced EMT, while H19 overexpression or a miR-370-3p knockdown promoted TGF-β-induced EMT. Mechanistically, H19 could directly bind to miR-370-3p and effectively act as its competing endogenous RNA. Furthermore, we demonstrated that this activity of H19 was involved in its promotion of TGF-β-induced EMT. Thus, our results may provide novel insights into the process of TGF-β-induced EMT.