位置:成果数据库 > 期刊 > 期刊详情页
沙利度胺增强X射线对胶质瘤U251细胞辐射敏感性机制的研究
  • 期刊名称:辐射研究与辐射工艺学报
  • 时间:0
  • 页码:368-371
  • 语言:中文
  • 分类:R73-3[医药卫生—肿瘤;医药卫生—临床医学] R739.41[医药卫生—肿瘤;医药卫生—临床医学]
  • 作者机构:[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
  • 相关基金:国家自然科学基金(30870585)和江苏省研究生创新基金(2010.8)资助
  • 相关项目:ON、SEMA3B和DCX抑制基因在脑胶质瘤生长及转移中的作用机理研究
中文摘要:

研究他莫昔芬(Tamoxifen,TAM)联合γ射线辐照对脑皎质瘤细胞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。

英文摘要:

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.

同期刊论文项目
同项目期刊论文