MicroRNA-153 regulated AKT1 expression and suppressed cell proliferation of epithelial ovarian cancer cells.

Epithelial ovarian cancer (EOC) is the most fatal malignancies in females worldwide, with increasing incidence recently in China. MiR-153 was reported to be dysregulated in some human cancers, including EOC. In this study, we explored the roles of miR-153 and its target AKT1 in regulating growth and migration in EOC. Cell proliferation was measured with a CCK-8 assay. Real-time quantitative RT-PCR was performed to investigate expression levels of miR-153. Cell cycle features were analyzed by Flow cytometry system. The direct target gene was confirmed by dual-luciferase reporter assay. We found the expression levels of miR-153 were generally lower in the EOC tissues than in the matched normal tissues. The miR-153 mimics caused significant G0/G1 arrest in A2780 cells. Overexpression of miR-153 suppressed cell proliferation and migration in ovarian cancer. Results of dual-luciferase reporter assay suggested that AKT1 was a direct target of miR-153 in ovarian cancer cells. Overexpression of AKT1 reverses the inhibition effect of miR-153 on cell proliferation. Introduction of miR-153 into EOC cell lines leaded to inhibition of cell proliferation and migration by directly targeting AKT1. MiR-153 may have prognostic or therapeutic value for the future management of ovarian cancer patients.
Competing Interests: None.
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