下调FAM111B对乳腺癌细胞增殖和凋亡的影响

The effects of down-regulation of FAM111B on cell proliferation and apoptosis in breast cancer

目的:探讨下调FAM111B对乳腺癌细胞系MDA-MB-231和MCF7细胞增殖和凋亡的影响及其机制。方法:构建siR-FAM111B慢病毒载体,转染乳腺癌MDA-MB-231和MCF7细胞,qRT-PCR检查转染组与对照组FAM111B mRNA表达,Western blotting法检测各组细胞FAM111B蛋白表达。用CCK-8法检测细胞的增殖能力。流式细胞术检测Annexin-V/PI双染各组细胞的凋亡情况。Western blotting法检测凋亡相关蛋白Bax和Bcl-2的表达。结果:siR-FAM111B成功转染MDA-MB-231和MCF7细胞,转染后应用qRT-PCR和Western blotting检测,结果显示,FAM111B mRNA与蛋白水平均下调。siR-FAM111B能抑制两种细胞的增殖。Annexin-V/PI双染结果显示,下调FAM111B诱导两种细胞凋亡。Western blotting结果显示,下调FAM111B可以促进两种细胞Bax的表达,抑制Bcl-2的表达。结论:下调FAM111B能够抑制乳腺癌细胞的增殖,通过调节线粒体凋亡通路诱导细胞凋亡。

Objective:To investigate the effect and possible mechanism of down-regulation of FAM111 B on cell proliferation and apoptosis in breast cancer cells.Methods:Down-regulation vector siR-FAM111 B was constructed and transfected into MDA-MB-231 and MCF7 cells.qRT-PCR and Western blotting methods were used to confirm the mRNA and protein expression of FAM111 B.Transfected cell proliferation was detected by CCK-8,and apoptosis was detected by flow cytometry with Annexin-V/PI double staining.The expressions of Bax and Bcl-2 was detected by Western blotting.Results:Both MDA-MB-231 and MCF7 cells were successfully transfected with siR-FAM111 B,and the expression level of FAM111 B was down-regulated.Down-regulation of FAM111 B inhibited the cell proliferation in MDA-MB-231 and MCF7 cells.Flow cytometry results showed that down-regulation of FAM111 B induced cell apoptosis.Moreover,Western blotting results showed that down-regulation of FAM111 B promoted the expression of Bax,but inhibited Bcl-2 expression.Conclusion:Down-regulation of FAM111 B inhibitedcell proliferation,and induced apoptosis through regulating the mitochondrial apoptosis pathway in breast cancer.