Mechanism of microRNA-152-3p-Mediated Regulation of Autophagy and Sensitivity in Paclitaxel-Resistant Ovarian Cancer Cells.

Abstract

Objective: The study investigated microRNA-152-3p-mediated autophagy and sensitivity of paclitaxel-resistant ovarian cancer cells.

Methods: The miR-152-3p mimics and miR-152-3p inhibitor were transfected in A2780 cells and A2780T cells, and the scrambled sequences were transfected as a negative control group, the transfection efficiency was detected by qPCR technology. MTT was used to detect the proliferation and IC50 value of the cells after transfection. The expression of target proteins in A2780 cells and A2780T cells were detected by qPCR; The expression of phosphatase and tensin homolog (PTEN) and ATG4D after transfection were analyzed by Western blot. The knockdown efficiency of PTEN was detected by reverse qRT-PCR, MTT and Western blot.

Results: The expression level of miR-152-3p in A2780T cells was 52-fold higher than that in A2780 cells according to the results of qPCR. Downregulation of miR-152-3p reversed PTX-induced autophagy, inhibited cell proliferation and apoptosis, and reduced drug resistance in A2780T cells. Moreover, PTEN appeared to be a potential target of miR-152-3p, and low expression levels of miR-152-3p increased PTX sensitivity by downregulating PTEN in vitro.

Conclusion: PTEN may be a novel therapeutic target gene for patients with PTX-resistant ovarian cancer. These findings provide a potential translational framework for developing novel therapeutic strategies to overcome paclitaxel resistance in ovarian cancer.