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目的:探讨组蛋白去乙酰化酶抑制剂(HDI)trichostatin A(TSA)对Ku70的乙酰化及其在TSA诱导结肠癌细胞凋亡中的作用。方法:以TSA处理结肠癌细胞HCT116和HT29细胞,采用免疫沉淀结合Western blot检测TSA对Ku70乙酰化的作用,流式细胞术检测TSA诱导的细胞凋亡,Western blot检测凋亡相关蛋白Bax和细胞色素c(cytochrom c)的转位和表达。结果:TSA可引起结肠癌HCT116和HT29细胞Ku70乙酰化,并与凋亡密切相关,与对照组相比,HCT116凋亡率(P=0.007)和HT29细胞凋亡率(P=0.005)均显著增高,免疫共沉淀检测到TSA处理细胞后,Bax和Ku70之间的相互作用减弱,表明TSA引起的乙酰化促进Bax从Bax-Ku70复合物中释放,Western blot结果显示TSA促进Bax由胞浆向线粒体转位,同时促进cytochrom c由线粒体向胞浆转位。结论:Ku70乙酰化作用介导了TSA诱导的结肠癌细胞凋亡。
AIM: To investigate the effect of histone deacetylase inhibitor (HDI) trichostatin A (TSA) on acetylation of Ku70 and its role in TSA-induced colon cancer cell apoptosis. Methods: Human colon cancer cells HCT116 and HT29 were treated with TSA. The effect of TSA on the acetylation of Ku70 was detected by immunoprecipitation and Western blot. TSA-induced apoptosis was detected by flow cytometry. The apoptosis-related protein Bax and cells Translocation and expression of cytochrom c. Results: TSA induced the acetylation of Ku70 in HCT116 and HT29 cells, and was closely related to apoptosis. Compared with the control group, the apoptosis rate of HCT116 (P = 0.007) and the apoptosis rate of HT29 cells (P = 0.005) were significantly higher The results showed that the TSA-induced acetylation promoted the release of Bax from Bax-Ku70 complex, and Western blot results showed that TSA promoted the translocation of Bax from cytoplasm to Mitochondrial translocation, while promoting cytochrom c translocation from the mitochondria to the cytoplasm. Conclusion: Ku70 acetylation mediated TSA-induced apoptosis of colon cancer cells.