告达庭对人胃癌细胞株SGC-7901细胞增殖和凋亡的调节作用

目的研究告达庭(caudatin)对SGC-7901胃癌细胞增殖与凋亡的调节作用及可能的分子机制。方法 MTT法检测告达庭对SGC-7901细胞增殖的影响;流式细胞术分析SGC-7901细胞周期的变化;细胞形态学、琼脂糖凝胶电泳及FITC-AnnexinⅤ/PI双标记检测对胃癌细胞凋亡的影响,免疫印迹实验检测细胞凋亡相关蛋白表达水平。结果可明显抑制SGC-7901细胞的增殖,且抑制作用呈时间和剂量依赖性;SGC-7901细胞经告达庭作用24h后,处于G1期的细胞数目增加,而G2期和S期的细胞数目明显减少,并发生明显的凋亡;调节Bcl-2家族相关因子的表达水平和活化caspase-9、caspase-3与告达庭诱导SGC-7901细胞凋亡相关。结论告达庭可抑制SGC-7901胃癌细胞的增殖并诱发凋亡,其分子机制可能与调节Bcl-2与Bax的平衡以及释放CytC,进而促进caspase-9、caspase-3和PARP的降解密切相关。

Effect of caudatin on cell proliferation and apoptosis in human gastric cancer cell line SGC-7901

Aim To investigate the inhibitive effects of caudatin,a C21 steroidal aglycone,on the human gastric cancer cell line SGC-7901 in vitro.Methods MTT assay and flow cytometry were used to evaluate SGC-7901 cell proliferation and cell cycle.DNA laddering assay and AnnexinV-FITC/PI were used to investigate cell apoptosis.Western blot analysis was used to evaluate the expression level of proteins involved in cell apoptosis.Results Caudatin inhibited SGC-7901 cell growth and induced G0/G1 phase arrest in a dose-dependent manner.Human gastric cancer cells treated with caudatin showed typical characteristics of apoptosis.By Western blot analysis,we found the level of Bcl-2 was down-regulated after caudatin treatment,whereas the protein level of Bax was up-regulated. Furthermore,caudatin-induced apoptosis was accompanied by the release of Cyt C and the activation of caspase-3,caspase-9,and Poly(ADP-Ribose) Polymerase(PARP) .Conclusion Caudatin inhibited the cell proliferation and induced apoptosis in SGC-7901 cells,and the key regulators include Bcl-2,caspase-3,and caspase-9.