HSP90抑制剂17-AAG对胃癌SGC-7901细胞生长周期和凋亡的影响

目的研究一种特异性的热休克蛋白90抑制剂17-丙烯胺基-17-去甲氧基格尔德霉素（17-AAG）对人胃癌细胞SGC-7901
细胞增殖和凋亡的影响，分析其可能的作用机制。方法应用MTT比色法检测不同浓度的17-AAG对胃癌SGC-7901细胞的生
长抑制率；荧光显微镜下观察PI染色的SGC-7901细胞凋亡形态学变化；采用流式细胞术检测SGC-7901细胞的细胞周期变化
及凋亡率变化；通过免疫组化检测胃癌SGC-7901 细胞中Fas 蛋白的表达。结果MTT 法显示17-AAG 能明显抑制胃癌
SGC-7901 细胞的生长增殖，呈时间、剂量依赖性；流式细胞仪细胞周期分析显示，17-AAG处理48 h后使SGC-7901 细胞发生
G2/M期阻滞，并有诱导SGC-7901细胞凋亡的作用；细胞免疫组化结果显示，SGC-7901细胞胞浆内有Fas表达，随着药物浓度的
加大，阳性表达率也逐渐增加。结论17-AAG 通过改变细胞周期、诱导其凋亡来抑制胃癌SGC-7901 细胞的增殖，上调
SGC-7901细胞中Fas蛋白的表达是诱导凋亡的作用机制之一。

Effects of HSP90 inhibitor 17-AAG on cell cycle and apoptosis of human gastric cancer cell lines SGC-7901

Objective To study the effect of the HSP90 inhibitor, 17-allylamino-17-demethoxygelda-namycin (17-AAG), on cell
proliferation and apoptosis of human cancer SGC-7901 cells and explore the mechanisms. Methods 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. Results 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 G2/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. Conclusion 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.