MiR-182 promotes cell proliferation, migration and invasion by targeting FoxF2 in endometrial carcinoma cells

miR-182 has been reported to be up-regulated in many tumors, including endometrial carcinoma (EC). However, effects of miR-182 on the development of EC and possible molecular mechanisms have not been fully reported. The purpose of this study was to investigate the function of miR-182 and its potential mechanism in EC cell line RL95-2. At first, the expression of miR-182 in RL95-2 cells was inhibited using miR-182 inhibitor and detected by qRT-PCR. The expression of its target FoxF2 was also changed using lentiviral-mediated over-expression vector or interfering RNA vector. Cell migration and invasion, cell cycle progress and colony formation of RL95-2 cells were examined and statistically analyzed after the inhibition of miR-182 and/or altered expression of FoxF2. The inhibition of miR-182 significantly increased the expression of FoxF2, decreased the numbers of migrated and invaded cells, as well as the number of colonized cells, induced cell cycle arrest to the G1 phase, and suppressed epithelial-mesenchymal transition. Lentiviral-mediated over-expression of FoxF2 showed similar functions to miR-182 inhibition, whereas lentiviral-mediated down-regulation of FoxF2 displayed the opposite effects. The effects of miR-182 inhibitor on cell proliferation, migration, and invasion were reversed when the expression of both miR-182 and FoxF2 were suppressed. Our findings indicate miR-182 acts as an oncogenic miRNA and promotes cell proliferation, migration, and invasion by targeting FoxF2 in EC.