MicroRNA-107 induces cell cycle arrests by directly targeting cyclin E1 in ovarian cancer

Deregulated expression of microRNAs plays oncogenic or anti-oncogenic roles in various cancers. However, expression of miR-107 was not consistent among several types of cancer, and the effect of miR-107 in ovarian cancer remains unclear. In this study, we found that expression miR-107 was significantly decreased in ovarian cancer patients and in cell lines. Ectopic expression of miR-107 suppressed cell proliferation and G1 phase to S transition of cell cycle, and was associated with downregulation of cyclin E1 (CCNE1) expression. Mechanistically, CCNE1 was confirmed to be a direct target of miR-107 through the dual-luciferase reporter assay. Knockdown of CCNE1 dramatically impeded cell cycle in G1/S phase transition similarly as miR-107 overexpression did. In addition, overexpression of CCNE1 reversed the inhibition of cell proliferation induced by miR-107 overexpression. Finally, miR-107 had anti-cancer potential by suppressing tumor initiation and progression in vivo. Our finding indicates that miR-107 serves as a tumor suppressor by decreasing CCNE1 expression levels, which may provide potential therapeutic strategies in ovarian cancer treatment. •Expression of miR-107 was decreased in ovarian cancer.•Elevated miR-107 suppressed cell proliferation and G1 phase to S transition of cell cycle.•Cyclin E1 was confirmed to be a direct target of miR-107.•miR-107 had anti-cancer potential by suppressing tumor initiation and progression in vivo.