中文摘要：

为了探讨Tip60对细胞DNA损伤修复及细胞周期的影响及其相关机制,通过在U2OS细胞中稳定转染外源Tip60基因,分析了细胞增殖能力及DNA双链断裂修复能力,以及辐射后引起的细胞周期阻滞和细胞周期相关蛋白表达变化。结果发现Tip60在U2OS细胞中的稳定表达降低了细胞增殖能力却提高了细胞DNA损伤修复能力,并通过引起电离辐射诱发CyclinB/CDC2复合物表达水平下降,导致细胞G2/M期阻滞延长。

英文摘要：

To investigate the effects of Tip60 on DNA damage repair,cell cycle and the related mechanism as well,the proliferative activity,DNA double strand break（DSB） repair competency and cell cycle arrest were analyzed in stable Tip60-overexpression U2OS cells established by transfecting with exogenous Tip60 gene.It was found that the overexpression of Tip60 inhibited the proliferative activity but increased the DNA damage repair competency.The radiation-induced G2/M arrest was prolonged in Tip60 over-expressed U2OS cells,which was associated with a decreasing level of cell cycle checkpoint protein Cyclin B/CDC2 complex.