CTAB对乳腺癌细胞MCF-7和MDA-MB-231凋亡影响

Effect of CTAB on apoptosis of breast cancer cells MCF-7 and MDA-MB-231

为探索十六烷基三甲基溴化铵(CTAB)对乳腺癌细胞凋亡的影响及其可能的作用机制,用不同浓度的CTAB作用于乳腺癌细胞系MCF-7和MDA-MB-231,经MTT实验证实,CTAB对乳腺癌细胞具有明显的杀伤作用.根据MTT实验结果确定CTAB对两种乳腺癌细胞的IC50值,通过显微镜观察根据IC50值设定浓度给药24 h对乳腺癌细胞引起的形态变化.然后根据MCF-7的IC50值设置浓度梯度进行AV-PI双染色凋亡流式细胞实验,检测不同浓度CTAB引起乳腺癌细胞凋亡的情况.最终通过Western Blot实验检测发现,乳腺癌细胞MCF-7经CTAB处理后P-bcl-2蛋白表达量降低,p53、Bax、Bim、Bad、Cleaved Caspase-3和Cleaved Caspase-9等凋亡相关蛋白的表达量升高.综上所述,CTAB可能通过激活p53信号通路诱导乳腺癌细胞线粒体内源性凋亡.

To explore the effect of cetyltrimethylammonium bromide(CTAB)on breast cancer cell apoptosis and its possible mechanism,CTAB with different concentrations is applied to MCF-7 and MDA-MB-231 cell lines.MTT experiment shows that CTAB has a significant killing effect on breast cancer cells.According to the results of MTT experiment,the IC50 values of CTAB on two kinds of breast cancer cells are determined.The morphological changes of breast cancer cells caused by the set concentrations according to IC50 after 24 h-treatment are observed by the microscope.Then,according to the IC50 value of MCF-7,the concentration gradient is set to carry out AV-PI double staining apoptosis flow cytometry to detect the apoptosis of breast cancer cells caused by different concentrations of CTAB.Finally,Western Blot experiment shows that the expression of P-bcl-2 protein decreases,and the expression of apoptosis-related proteins such as p53,Bax,Bim,Bad,Cleaved Caspase-3 and Cleaved Caspase-9 increases in breast cancer cell MCF-7 treated with CTAB.In conclusion,it is shown that CTAB may activate mitochondrial endogenous apoptosis of breast cancer cells by activating p53 signaling pathway.