Abstract:Objective To study the effects of microRNA (miR)-324-3p on the radiosensitivity of breast cancer MCF-7 cells cultured in vitro and its mechanism. Methods The expression levels of miR-324-3p and serine/threonine protein kinase (AKT)1 were respectively detected by qRT PCR and Western blot. The overexpressed mir-324-3p mimics, silenced and overexpressed AKT1 plasmids were transfected into breast cancer MCF-7 cells by lipofectamine2000 and irradiated with 4 Gy. The cell survival fraction,cell viability,apoptosis rate were determined by colony formation assay,cell counting kit 8 assay(CCK-8 kit)and flow cytometry,respectively,and the fitting curve of click multi-target model was drawn.TargetScan online prediction,luciferase reporter gene assay and Western blot were used to verify the target orientation of miR-324-3p. Results Compared with normal mammary epithelial cells line MCF10A,the expression of miR-324-3p were down-regulated,and the expression of AKT1 protein were up-regulated in MDA-MB-435S and MCF-7 breast cancer cells(all P<0.05).Overexpression of miR-324-3p combined with radiation increased radiosensitivity of MCF-7 cells,decreased survival rate in a dose-dependent manner and cell activity,and increased the apoptosis rate (all P<0.05).MiR-324-3p targeting AKT1 expression,when silencing AKT1 combined with radiation,the radiosensitivity of MCF-7 cells increased,survival fraction decreased in a dose-dependent manner cell activity decreased,and the apoptosis rate of MCF-7 cells increased (all P<0.05).Overexpression of AKT1 reversed the effect of miR-324-3p on radiosensitivity,cell proliferation and apoptosis of breast cancer. Conclusion Overexpression of miR-324-3p can target the regulation of AKT1 expression and enhance the radiosensitivity of breast cancer MCF-7 cells.