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.