mTORC1/2抑制剂PP242诱导胶质瘤细胞凋亡及其初步机制  

Apoptosis of glioma cells induced by mTORC1/2 inhibitor PP242 and its primary mechanism

作　　者：赵斌[1] 张青青[1] 马文彬[1] 郭伟[1] ZHAO Bin;ZHANG Qingqing;MA Wenbin;GUO Wei(Department of Neurology,Affiliated Hospital of Binzhou Medical College,Binzhou 256603,China)

机构地区：[1]滨州医学院附属医院神经内科

出　　处：《汕头大学医学院学报》2019年第4期206-209,共4页Journal of Shantou University Medical College

摘　　要：目的:探讨m TORC1/2抑制剂PP242对人胶质瘤细胞U251凋亡的影响及其机制。方法:用不同浓度的PP242处理胶质瘤U251细胞不同时间后,CCK8法测定细胞存活率,采用流式细胞术检测细胞凋亡情况,Western blot检测凋亡通路相关蛋白的变化。结果:PP242呈时间和浓度依赖性地抑制人胶质瘤细胞的生长,促进细胞凋亡。同时PP242促进caspase依赖的凋亡,使Bax、cleaved caspase-3和cleaved caspase-9等蛋白表达上调,Bcl-2表达下调。结论:mTORC1/2抑制剂PP242通过调控凋亡蛋白的表达来诱导胶质瘤细胞的凋亡。Objective:To investigate the effect of mTORC1/2 inhibitor PP242 on apoptosis of human glioma cell line U251 and its mechanism. Methods: After the glioma U251 cells were treated with different concentrations of PP242 for different times,the cell survival rate was measured by CCK8 method,apoptosis was detected by flow cytometry, and apoptosis pathway related proteins were detected by Western blot.Results: PP242 inhibited the growth of human glioma cells and promoted apoptosis in a time and concentration dependent manner. At the same time,PP242 promoted caspase dependent apoptosis,increased the expression of Bax, cleaved caspase-3 and cleaved caspase-9, and decreased the expression of Bcl-2.Conclusion: mTORC1/2 inhibitor PP242 induces apoptosis of glioma cells by regulating the expression of apoptotic proteins.

关 键 词：MTOR 胶质瘤 凋亡 PP242 

分 类 号：R739.41[医药卫生—肿瘤]