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作 者:杨彩玲[1] 崔卫刚[2] 张应花[2] 路德荣 刘进忠[4]
机构地区:[1]新乡医学院第一附属医院口腔外科,新乡453100 [2]新乡医学院人体解剖学教研室,新乡453003 [3]新乡医学院第三附属医院消化内科,新乡453003 [4]郑州大学口腔医学院口腔病理教研室,郑州450052
出 处:《安徽医科大学学报》2014年第10期1379-1382,共4页Acta Universitatis Medicinalis Anhui
基 金:河南省教育厅科学技术研究重点项目(编号:14B320018)
摘 要:目的利用涎腺腺样囊性癌细胞系ACC-M细胞为模型,研究不同浓度埃克替尼(icotinib)对涎腺腺样囊性癌细胞系ACC-M细胞凋亡的影响以及线粒体在icotinib诱导ACC-M细胞凋亡中的作用。方法 icotinib和P53抑制剂(PFT)分别处理ACC-M细胞,应用噻唑蓝比色法检测细胞活性,利用Western blot法检测P53和胞质内细胞色素C(Cyt C)蛋白的表达变化,用Caspase-3凋亡相关蛋白活力检测ACC-M细胞的凋亡情况。结果 icotinib可抑制ACC-M细胞的活性,增加胞质Cyt C蛋白的表达和P53在线粒体的转位并诱导ACC-M细胞凋亡。用PFT预处理后,icotinib诱导ACC-M细胞的凋亡明显下降,线粒体蛋白P53的表达降低,胞质内Cyt C表达减少,Caspase-3凋亡相关蛋白活力下降。结论 icotinib可能通过诱导P53转位到线粒体进而促进ACC-M细胞凋亡。Objective To investigate the role of mitochondrion in the induction of the apoptosis in human salivary adenoid cystic carcinoma cells through icotinib and to observe the effect of different concentrations of icotinib on the apoptosis. Methods The ACC-M cells were exposed to icotinib and ( or) the P53 inhibitor PFT. The cell viability of ACC-M was measured by MTT assay. Expression of P53 and Cyt C was determined by Western blot analysis. The apoptosis of ACC-M cells was measured by Caspase-3 apoptosis related protein activity. Results icotinib inhib-ited the viability in ACC-M. icotinib significantly increased the protein levels of P53 in mitochondrion and Cyt C in cytoplasm and induced apoptosis in ACC-M. However, pretreatment with P53 inhibitor( PFT) , the inhibitory effect of icotinib on ACC-M cells was significantly reversed. The level of the Caspase-3 apoptosis related protein activity and the expression of P53 in mitochondrion and Cyt C in cytoplasm were also decreased significantly. Conclusionicotinib may induce apoptosis of ACC-M through the P53 mitochondrial translocation.
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