他莫昔芬联合^(60)Co γ射线辐照下调脑胶质瘤细胞PKCα蛋白表达的实验研究  

Study on the down-regulation of PKCα by tamoxifen combined with ^(60)Co γ-irradiation in glioma cells

作　　者：尹小祥[1,2] 刘海燕[1] 冯爽[1] 马燕[1] 张昊文[1] 刘芬菊[1] 

机构地区：[1]苏州大学放射医学与公共卫生学院,苏州215123 [2]江苏省泰兴市人民医院放疗科,泰兴225400

出　　处：《辐射研究与辐射工艺学报》2011年第1期28-32,共5页Journal of Radiation Research and Radiation Processing

基　　金：国家自然科学基金(30870585);江苏省研究生创新基金(2010.8)资助

摘　　要：研究他莫昔芬(Tamoxifen,TAM)联合γ射线辐照对脑胶质瘤细胞PKCα蛋白表达的影响,初步探讨TAM降低辐射抗性的机制。采用Western-Blot法检测PKCα和G1期调控蛋白CylinD1的表达;碱性单细胞凝胶电泳法检测DNA链断裂。结果提示,TAM联合γ射线辐照可诱导PKCα蛋白和CyclinD1蛋白表达量降低,增加单纯照射对DNA的损伤并抑制其修复。结果提示,TAM联合γ射线辐照能够增强TAM或辐照单独处理对PKCα蛋白表达的下调、诱导CyclinD1低表达和抑制DNA损伤修复,与TAM降低SHG-44细胞的辐射抗性有关。The mechanism of radio-sensitizing effect of tamoxifen on the influence of PKCα expression has been explored by tamoxifen combined with 60↑Coγ-irradiation in human glioma ceils. The protein expression of PKCα and CyclinD 1 were detected by using Western-Blot. The level of DNA strand breaks was detected by the alkaline single-cell gel electrophoresis assay. The results demonstrated that the conabination of tamoxifen and 60↑Coγ-irradiation could reduce the expression of PKCα and CyclinD1 .And it also enhanced the radiation-induced DNA damage and attenuated the repair of damaged DNA. The above results reveal that the combination of tamoxifen and 60↑Coγ-irradiation can enhance the downregulation of the expression of PKCα and the induction in the low expression of CyclinD1 as well as the delay of DNA repair. All these may be related to the impairment of the radioresistance of SHG-44 cells by tamoxifen.

关 键 词：他莫昔芬 脑胶质瘤 蛋白激酶CΑ CYCLIND1 DNA损伤 辐射抗性 

分 类 号：R73-3[医药卫生—肿瘤] R739.41[医药卫生—临床医学]