Mechanism of miR-506-3p regulating breast cancer cell proliferation,apoptosis and its resistance to docetaxel
Objective This study investigates the effect and molecular mechanism of miR-506-3p on breast cancer cell prolif-eration,apoptosis and its resistance to docetaxel.Methods MCF-10A cells and breast cancer cell lines MDA-MB-231,MCF-7,BT549 were cultured in vitro.In MDA-MB-231 cells,miR-506-3p mimics,TUBA1C small interfering RNA or TUBA1C overexpressing plasmid were transfected,or TUBA1C overexpressing plasmid and miR-506-3p mimics were co-transfected.Real-time fluorescent quantitative PCR(RT-qPCR)was used to detect the expression of miR-506-3p and TUBA1C mRNA;methyl thiazolyl tetrazolium as-say(MTT)was used to detect cell proliferation and half inhibitory concentration(IC50);flow cytometry was used to detect cell apopto-sis;dual luciferase reporter experiment was used to detect targeting relationship of miR-506-3p and TUBA1C.Results Compared with MCF-10A cells,the expression of miR-506-3p in MDA-MB-231,T47D and BT549 cells was decreased,and the expressions of TUBA1C mRNA and protein were increased(P＜0.05).After high expression of miR-506-3p or low expression of TUBA1C,the activity of MDA-MB-231 cells was decreased,apoptosis rate was increased,and IC50 value was decreased(P＜0.05).miR-506-3p targets and regulates TUBA1C;overexpression of TUBA1C reverses the effects of high expression of miR-506-3p on the proliferation and apoptosis of breast cancer cells MDA-MB-231 and the resistance to docetaxel.Conclusion The high expression of miR-506-3p may inhibit breast cancer cell proliferation,promote cell apoptosis and reduce the resistance of breast cancer cells to docetaxel by targeting and down-regulating TUBA1C.
miR-506-3palpha-tubulin specific 1c chainbreast cancerproliferationapoptosisdocetax-eldrug resistance
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