693201

MIR616

MicroRNAs, which can post-transcriptionally regulate gene expression by binding to the 3'-untranslated regions of the mRNAs, have been found to be the critical regulators of the development and progression of hepatocellular carcinoma (HCC). The present study demonstrated for the first time that microRNA-616 (miR-616) was markedly upregulated in HCC tissues, and was associated with the recurrence and metastasis of HCC. Elevated level of miR-616 was correlated with adverse clinicopathological features and poor prognosis of HCC patients. Gain- and loss-of-function studies revealed that miR-616 could potentiate the migration, invasion and the epithelial-mesenchymal transtion (EMT) phenotype of HCC cells. Phosphatase and tensin homolog (PTEN), the predicted target of miR-616 by bioinformatics analysis, was confirmed as a direct downstream target of miR-616 through western blotting, luciferase reporter and immunohistochemical assays. Furthermore, we demonstrated that miR-616 exerted the promoting effects on EMT and metastatic ability of HCC cells through suppressing PTEN expression. Based on these results, we conclude that miR-616 is a promising prognostic biomarker of HCC and targeting miR-616 may be a potential option to prevent the progression of HCC.

MicroRNAs (miRNAs), a group of short (~20 nt) noncoding RNAs, play critical roles in the development and progression of ovarian cancer (OC). The role of miR616, a recently identified cancer-associated miRNA, has never been examined in OC before. The present study demonstrated that the level of miR616 was increased in OC tissues. A high miR616 level was associated with poor tumor differentiation and advanced tumor-node-metastasis (TNM) stage. Survival analysis revealed that an elevated level of miR616 was associated with poor prognosis of OC patients as demonstrated by decreased overall survival (OS) and diseasefree survival (DFS). Overexpression of miR616 promoted the migration, invasion as well as epithelial-mesenchymal transition (EMT) of A2780 cells. Knockdown of miR616 inhibited these biological functions. Immunohistochemical (IHC) staining revealed that OC tissues with high miR616 levels exhibited a significantly decreased level of Ecadherin and an increased level of Ncadherin. Furthermore, tissue inhibitor of metalloproteinases 2 (TIMP2) was confirmed to be a direct downstream target of miR616. Inhibition of TIMP2 expression was required for the promoting effects of miR616 on the metastasis and EMT of OC cells. Collectively, this study revealed that miR616 promoted the progression of OC by enhancing cell migration, invasion and EMT.