Open AccessmiR‑31‑5p may enhance the efficacy of chemotherapy with Taxol and cisplatin in TNBC
Author(s) -
Xiaowei Shen,
Jiaqi Lei,
Lixin Du
Publication year - 2019
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2019.8191
Subject(s) - cisplatin , apoptosis , cancer research , microrna , flow cytometry , oncogene , chemotherapy , triple negative breast cancer , transfection , cell cycle , cell , cell growth , biology , cell culture , chemistry , cancer , breast cancer , microbiology and biotechnology , gene , biochemistry , genetics
The limited efficacy of chemotherapy with Taxol (TAX) and cisplatin (DDP) in triple-negative breast cancer (TNBC) has prompted the investigation of combined therapies. Previous studies demonstrated that microRNA (miR)-31-5p is involved in various biological processes. In the present study, it was hypothesized that the overexpression of miR-31-5p may enhance the efficacy of chemotherapy. The expression levels of miR-31-5p in the TNBC cell lines MDA-MB-231 and MDA-MB-468 were measured using reverse transcription-quantitative PCR following transfection with miR-31-5p mimic or inhibitor. A Cell Counting Kit-8 and flow cytometry assays suggested that the overexpression of miR-31-5p inhibited cell proliferation and promoted apoptosis, and these effects were reversed by transfecting a miR-31-5p inhibitor into MDA-MB-231 and MDA-MB-468 cells. Furthermore, the overexpression of miR-31-5p increased the sensitivity of cells to chemotherapy, which exhibited an increase in apoptosis and in the expression level of Bax, and a decrease in the expression level of Bcl-2. Chemotherapy resistance induced by miR-31-5p inhibitor could be reversed by inhibiting the AKT signaling pathway in MDA-MB-231 and MDA-MB-468 cells. In conclusion, the present preclinical results indicated that targeting miR-31-5p may enhance the efficacy of TAX- and DDP-mediated chemotherapy in TNBC.