MicroRNA-101 inhibits growth and metastasis of human ovarian cancer cells by targeting PI3K/AKT

8Citations
Citations of this article
8Readers
Mendeley users who have this article in their library.

Abstract

Introduction: Ovarian cancer is the most frequent cause of gynecological cancer related mortality in woman. This study was designed to investigate the role and therapeutic potential of miRNA-101 in ovarian cancer. Material and methods: Expression analysis was carried out by real-time quantitative polymerase chain reaction. Transfections were performed with the help of Lipofectamine 2000 reagent. AO/EB and annexin V/PI staining was used to detect apoptosis and flow cytometry was used for cell cycle analysis. Western blotting was employed for cell cycle analysis. Results: It was found that miRNA-101 was significantly down-regulated in ovarian cancer cells. The over-expression of miRNA-101 causes a significant decrease in the viability of ovarian cancer cells via the initiation of apoptosis and sub-G1 arrest of OVACAR-3 cells. It was indicated that PTEN was the potential target of miRNA-101 in OVACAR-3 cells. There was 4.5-fold up-regulation of PTEN expression in ovarian cancer cell lines and the over-expression of miRNA-101 in OVACAR-3 cells resulted in the down-regulation of PTEN expression. The inhibition of PTEN in the OVACAR-3 cells arrested the proliferation of these cells. The over-expression of miRNA-101 causes significant down-regulation in PI3K and AKT expression of OVACAR-3 cells. Conclusions: It can be concluded that miRNA-101 acts as a tumor suppressor which may be beneficial in the treatment of ovarian cancer.

Cite

CITATION STYLE

APA

Wei, M., Jin, H., Yang, S. L., Li, Z., Wang, X., Li, L. X., … Cui, M. H. (2021). MicroRNA-101 inhibits growth and metastasis of human ovarian cancer cells by targeting PI3K/AKT. Archives of Medical Science, 17(1), 127–134. https://doi.org/10.5114/aoms.2019.85404

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free