曲古抑菌素A对结肠癌细胞HCT116的作用及机制  

Effect of Trichostatin A on the human colon carcinoma HCT116 cells

作　　者：王丽[1] 刘晓燕[1] 李娟[1] 杨志惠[2] 

机构地区：[1]泸州医学院医学分子生物学实验室,泸州646000 [2]泸州医学院病理学教研室,泸州646000

出　　处：《四川解剖学杂志》2012年第1期4-6,共3页Sichuan Journal of Anatomy

基　　金：四川省科技厅科研项目(No.07JY029-134);四川省教育厅科研项目(No.07ZB110)

摘　　要：目的通过组蛋白去乙酰化酶(histone deacetylase,HDACs)抑制剂曲古抑菌素A(TSA)对人结肠癌细胞HCT116增殖与凋亡作用的研究,探讨TSA对结肠癌的作用机制。方法:应用四氮唑蓝(MTT)法、Hoechst染色法、Western blot法和光学显微镜观察经不同浓度TSA处理后的HCT116增殖、凋亡与相关蛋白的改变。结果:TSA可时间依赖性地抑制HCT116细胞生长,促进凋亡,但浓度依赖性不明显。与对照组相比,TSA作用时,脆性组氨酸三联体(FHIT)和Bax蛋白的表达均出现一定程度增加,而骨桥蛋白(OPN)的表达出现一定程度的降低,AKT蛋白表达变化不明显。结论:TSA可抑制结肠癌细胞HCT116增殖,促进其凋亡,其机制可能与上调FHIT和Bax的表达,下调OPN表达有关。Objective To investigate the effect of trichostatin A（TSA） on colon carcinoma,and to explore the mechanism of TSA on the proliferation and apoptosis of human colon carcinoma cell HCT116.Methods MTT,Hoechst,Western blot and optical microscope were conducted to observe the alteration of cell proliferation,apoptosis of HCT116 after treated with TSA.Results The proliferation of HCT116 was inhibited by TSA in a time-dependent manner while not in dose dependent manner.TSA induced the apoptosis of HCT116 cells by increasing the expressions of fragile histidine triad（FHIT） and Bax,decreasing the expressions of Osteopontin（OPN）.Conclusion The proliferation of HCT116 cells could be inhibited by TSA,the mechanisms of cell apoptosis maybe relate to upregulating FHIT,Bax expression and downregulating OPN expression.

关 键 词：结肠癌 古抑菌素A 细胞凋亡 脆性组氨酸三联体 骨桥蛋白 

分 类 号：R735.35[医药卫生—肿瘤]