Mechanism of RMST promoting drug resistance to TAC sequential regimen in breast cancer

AimTo construct a stable RMSToverexpressing breast cancer MCF-7 cell line and investigate the effect of RMST on the therapeutic efficacy of the TAC sequential regimen in breast cancer, as well as to explore its underlying mechanisms.MethodsThe primers were designed based on RMST (NR_186054. 1) sequence, and the XhoI/EcoRI restriction enzyme vector was constructed to prepare the lentivirus to infect MCF-7 cells. MCF-7 cells were divided into OE-NC (empty vector) and OE-RMST (overexpression) groups. RMST expression was verified by qRT-PCR. Cell viability and IC50 were measured by CCK-8 assay. Proliferation was assessed by plate colony formation, migration by scratch assay, invasion by Transwell assay, apoptosis by flow cytometry. The mRNA and protein expressions of drug resistance, apoptosis proteins and key molecules of the Wnt/β -catenin signaling pathway were detected by qRT-PCR and Western blot.ResultsCompared with the OE-NC group, the expression of RMST in the OERMST group significantly increased (P P P P P P P P P ConclusionThe RMST overexpression MCF-7 cell line is successfully constructed, which confirms that RMST may promote the resistance of MCF-7 cells to TAC sequential regimen by activating Wnt/β-catenin pathway.