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As small non-coding RNA molecules, microRNAs (miRs) function in the regulation of tumorigenesis. Proliferation in ovarian cancer is considered to be associated with miR-16; however, the role of miR-16 in the migration and invasion of ovarian cancer cells remains unclear. The results of the present study demonstrated that miR-16 expression is downregulated in the ovarian cancer SKOV3 and OVCAR3 cell lines compared with that in normal ovarian epithelial cells (OECs). miR-16 overexpression inhibited the proliferation, migration and invasion of SKOV3 and OVCAR3 cells, and decreased the expression of matrix metallopeptidase (MMP)2 and MMP9. Additionally, miR-16 upregulated the expression of cadherin 1, an intercellular adhesion molecule, and downregulated the expression of some mesenchymal markers, including snail family transcriptional repressor 2, snail family transcriptional repressor 1, Vimentin, twist family BHLH transcription factor 1 and cadherin 2 in SKOV3 and OVCAR3 cells. Furthermore, it was indicated that miR-16 overexpression in SKOV3 and OVCAR3 cells resulted in a significant increase in anti-glycogen synthase kinase 3 β expression and a decrease in the expression of Wnt family member 3A, β-catenin, MYC proto-oncogene, BHLH transcription factor and cyclin D1 compared with the NC group. The results of the present study indicated that miR-16 exerts a suppressive effect on cell migration and invasion in ovarian cancer in vitro , through inactivation of the Wnt/β-catenin signaling pathway. The data suggest that miR-16 may be a potential therapeutic agent for the treatment and prevention of ovarian cancer.

MicroRNA‑16 inhibits migration and invasion via regulation of the Wnt/β‑catenin signaling pathway in ovarian cancer