miR-96 enhances the proliferation of cervical cancer cells by targeting FOXO1.

MiRNAs affect various biological pathways associated with the development, progression, clinical outcome and treatment response improvement in cervical cancer. This study was performed to evaluate the effects of miRNA 96 on cervical cancer and to clarify the mechanism. Vivo and vitro experiments were conducted in our trial. MiR-96 is upregulated in cervical cancer cell lines and cervical cancer tissues and is correlated with clinical features in cervical cancer patients. Overexpression of miR-96 enhances proliferation of cervical cancer cells, while inhibiting miR-96 reduces the proliferation of cervical cancer cells. Inhibition of miR-96 significantly decreased the percentage of cells in the S phase and increased the percentage of cells in G1/G0 peak in both SiHa and CaSki cells compared with NC cells and decreased the expressions of p21, p27 and cyclin D1. FOXO1 3'-UTR was sub cloned into a luciferase reporter vector and the putative miR-96 binding site in the FOXO1 3'-UTR was mutated. Treated with miR-96 inhibitor consistently enhanced the luciferase activity of the FOXO1 3'-UTR luciferase reporter plasmids in both SiHa and CaSki cells, whereas mutations in the miR-96-binding site abolished the effect. Vivo experiment also support these results. Therefore, inhibition of miR-96 might suppress growth, proliferation of CC cells and promote apoptosis of CC cells both in vitro and in vivo.