MiR-361-5p decreases the tumorigenicity of epithelial ovarian cancer cells by targeting at RPL22L1 and c-Met signaling.

A large number of studies have shown that miRNAs are important regulators of epithelial-to-mesenchymal transition (EMT) and are associated with metastasis in epithelial ovarian cancer (EOC). MiR-361-5p has been shown to play pivotal roles in tumorigenesis and metastasis; however, a role for miR-361-5p in EOC has not been reported. In this study, we found that miR-361-5p was significantly down-regulated in EOC tissues and cell lines. In addition, over-expression of miR-361-5p inhibited the migration and invasion of EOC cells in vitro. MiR-361-5p influenced the expression of the EMT-associated proteins by upregulating the epithelial marker E-cadherin and downregulating the mesenchymal markers, N-cadherin and vimentin. Further studies identify miR-361-5p directly targeted Ribosomal L22-like1 (RPL22L1) and c-Met. Moreover, miR-361-5p repressed the Akt/mTOR pathway after c-Met inhibition. Reintroduction of RPL22L1 and c-Met reversed miR-361-5p-induced EMT suppression. Consistently, inverse correlations were also observed between the expression of miR-361-5p and RPL22L1 or c-Met in human EOC tissue samples. Taken together, miR-361-5p inhibited the EMT progression in EOC cells by targeting RPL22L1 and c-Met/Akt/mTOR signaling. IJCEP