miR-183 modulated cell proliferation and apoptosis in ovarian cancer through the TGF-β/Smad4 signaling pathway.

An increasing body of evidence has revealed that the aberrant expression of microRNAs (miRNAs/miRs) is involved in the development and progression of ovarian cancer (OC). miR‑183 has been demonstrated to act as a tumor suppressor and oncogene in various types of human cancers. However, the biological role of miR‑183 in OC still remains unclear. The aim of the present study was to investigate the role of miR‑183 and evaluate its underlying mechanism in OC. In the present study, miR‑183 was observed to be upregulated in OC tissues and cell lines as determined by reverse transcription‑quantitative polymerase chain reaction. The effects of miR‑183 on OC were further investigated via western blotting, MTT, wound healing, Transwell and immunofluorescence analyses. Downregulation of miR‑183 markedly inhibited cell proliferation, migration and invasion, and promoted apoptosis in OC cells. Furthermore, it was initially confirmed that mothers against decapentaplegic homolog 4 (Smad4) was identified as an efficient target of miR‑183 by luciferase activity assay. Finally, the results revealed that miR‑183 directly regulated biological function via the transforming growth factor (TGF)‑β/Smad4 signaling pathway in OC cells. In conclusion, the results of the present study suggested that miR‑183 exerted tumor‑promoting roles in OC, at least partially by regulating Smad4 via the TGF‑β/Smad4 signaling pathway. Therefore, miR‑183 may serve as a potential target for the diagnosis and prognosis of OC.