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.
Keywords: AKT1; Epithelial ovarian cancer; microRNA-153.
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