Chen Meini, Xu Jinghong, Zhao Jumei
Yanan Medical College, Yanan University, Yanan, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2013 Feb;33(2):271-5.
To study the effect of the HSP90 inhibitor, 17-allylamino-17-demethoxygeldanamycin (17-AAG), on cell proliferation and apoptosis of human cancer SGC-7901 cells and explore the mechanisms.
The inhibitory effect of 17-AAG on the proliferation and morphology of SGC-7901 cells was assessed with MTT assay and DNA-PI staining, respectively. Flow cytometry was employed to analyze the changes in cell cycle and apoptosis of the cells following 17-AAG exposure. The cellular expression of Fas protein was detected by immunohistochemistry.
17-AAG significantly suppressed the proliferation of SGC-7901 cells in a time- and dose-dependent manner. After treatment with 17-AAG for 48 h, SGC-7901 cells showed cell cycle arrested at G(2)/M stage, and the cell apoptosis rate increased with the 17-AAG concentration. The expression of Fas protein in the cytoplasm of SGC-7901 cells increased gradually with the increase of 17-AAG concentration.
17-AAG can induce apoptosis, alters the cell cycle distribution and up-regulates the expression of Fas protein in SGC-7901 cells to suppress the cell proliferation.
研究热休克蛋白90(HSP90)抑制剂17-烯丙基氨基-17-去甲氧基格尔德霉素(17-AAG)对人胃癌SGC-7901细胞增殖和凋亡的影响,并探讨其作用机制。
分别采用MTT法和DNA-PI染色法评估17-AAG对SGC-7901细胞增殖和形态的抑制作用。采用流式细胞术分析17-AAG作用后细胞周期和凋亡的变化。通过免疫组织化学检测细胞中Fas蛋白的表达。
17-AAG能显著抑制SGC-7901细胞的增殖,且呈时间和剂量依赖性。17-AAG作用48小时后,SGC-7901细胞的细胞周期阻滞于G(2)/M期,细胞凋亡率随17-AAG浓度的增加而升高。SGC-7901细胞胞质中Fas蛋白的表达随17-AAG浓度的增加而逐渐升高。
17-AAG可诱导SGC-7901细胞凋亡,改变细胞周期分布,上调Fas蛋白表达,从而抑制细胞增殖。