Abstract
MicroRNAs (miRNAs), a group of short (~20 nt) non‑coding RNAs, play critical roles in the development and progression of ovarian cancer (OC). The role of miR‑616, a recently identified cancer-associated miRNA, has never been examined in OC before. The present study demonstrated that the level of miR‑616 was increased in OC tissues. A high miR‑616 level was associated with poor tumor differentiation and advanced tumor-node-metastasis (TNM) stage. Survival analysis revealed that an elevated level of miR‑616 was associated with poor prognosis of OC patients as demonstrated by decreased overall survival (OS) and disease‑free survival (DFS). Overexpression of miR‑616 promoted the migration, invasion as well as epithelial-mesenchymal transition (EMT) of A2780 cells. Knockdown of miR‑616 inhibited these biological functions. Immunohistochemical (IHC) staining revealed that OC tissues with high miR‑616 levels exhibited a significantly decreased level of E‑cadherin and an increased level of N‑cadherin. Furthermore, tissue inhibitor of metalloproteinases 2 (TIMP2) was confirmed to be a direct downstream target of miR‑616. Inhibition of TIMP2 expression was required for the promoting effects of miR‑616 on the metastasis and EMT of OC cells. Collectively, this study revealed that miR‑616 promoted the progression of OC by enhancing cell migration, invasion and EMT.