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机构地区:[1]哈尔滨医科大学附属肿瘤医院检验科,黑龙江省哈尔滨市150081 [2]哈尔滨医科大学第二临床医学院普外科,黑龙江省哈尔滨市150086
出 处:《世界华人消化杂志》2010年第23期2469-2471,共3页World Chinese Journal of Digestology
基 金:哈尔滨医科大学第二临床医学院博士科研基金资助项目;No.BS2008-05
摘 要:目的:探讨组蛋白去乙酰化酶(HDAC)抑制剂曲古菌素A(TSA)对胃癌细胞系SGC-7901中组蛋白H3乙酰化水平及细胞凋亡的影响.方法:流式细胞仪检测细胞凋亡率,免疫细胞化学法检测75μg/LTSA干预前胃癌细胞系SGC-7901中乙酰化组蛋白H3的表达.结果:TSA干预后胃癌细胞系SGC-7901中乙酰化组蛋白H3的表达水平明显升高,乙酰化组蛋白H3阳性细胞数从1.12±1.06上升至35.43±6.05,与未干预相比两者表达有显著性差异(P<0.01),流式细胞仪分析显示细胞凋亡率增加到22.13%±3.49%.结论:TSA可诱导细胞凋亡,促进胃癌细胞系SGC-7901中乙酰化组蛋白H3的表达.AIM:To investigate the effects of trichosttain A(TSA),a histone deacetylase inhibitor,on apoptosis in hunman gastric cancer cell line SGC-7901.METHODS:After SGC-7901 cells were incubated with 75 μg/L TSA for 48 h,cell apoptosis was measured by flow cytometry,and the expression of acetylated histone H3 was detected by immunohistochemistry.RESULTS:TSA could significantly inhibit proliferation and induce apoptosis of SGC-7901 cells.The expression level of acetylated histone H3 was higher in SGC-7901 cells treated with TSA(75 μg/L for 48 h) than in control cells(35.43 ± 6.05 vs 1.12 ± 1.06).The apoptosis rate was significantly different between SGC-7901 cells treated with TSA(75 μg/L for 48 h) and control cells(P 0.05).CONCLUSION:TSA can induce SGC-7901 cell apoptosis possibly by up-regulating the expression of acetylated histone H3.
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