miR‑210‑3p regulates cell growth and affects cisplatin sensitivity in human ovarian cancer cells via targeting E2F3

Abstract

The potential role of microRNA (miR)-210-3p in carcinogenesis and the cisplatin sensitivity of ovarian cancer were evaluated in the present study. The relative expression levels of miR-210-3p in cisplatin-sensitive SKOV-3 cells and cisplatin-resistant SKOV-3/DDP cells were determined using reverse transcription-quantitative polymerase chain reaction analysis. miR-210-3p mimics and inhibitors were transfected into SKOV-3/DDP cells. Cell Counting Kit-8, scratch and Transwell invasion assays and flow cytometry were conducted to evaluate the role of miR-210-3p in ovarian cancer cells. A luciferase reporter assay was used to verify the association between miR-210-3p and E2F transcription factor 3 (E2F3). Drug sensitivity was evaluated by treating the cells with cisplatin. The expression level of miR-210-3p was lower in SKOV-3/DDP cells than in SKOV-3 cells. Compared with the untransfected control, SKOV-3 cells transfected with miR‑210‑3p exhibited a significantly higher survival rate. The overexpression of miR-210-3p inhibited SKOV-3/DDP cell proliferation, migration and invasion, and promoted cell apoptosis. By contrast, the inhibition of miR-210-3p promoted cell migration and invasion. The luciferase reporter assay confirmed that E2F3 was a direct target gene of miR-210-3p. Cisplatin treatment resulted in a sharp decrease in the survival rate of SKOV-3/DDP cells transfected with the miR-210-3p mimics. The decrease in cell survival rate caused by the overexpression of miR-210-3p was rescued by the overexpression of E2F3 in SKOV-3/DDP cells. Taken together, these results suggest that miR-210-3p may act as a tumor suppressor in ovarian cancer cells and affect the sensitivity of cells to cisplatin by directly targeting E2F3. This indicates its potential use as a therapeutic target for improving drug resistance in ovarian cancer.