天花粉蛋白抑制胃癌细胞生长及其分子机制研究

The Anti-tumor Effect of Trichosanthin on Gastric Cancer Cell and Its Molecular Mechanism

目的观察天花粉蛋白(trichosanthin,TCS)对人胃癌细胞SGC7901诱导凋亡的作用及机制。方法应用荧光显微镜观察0、7、14、28μmol/L TCS对SGC7901细胞形态学的影响及细胞计数。应用流式细胞仪测定各浓度TCS对SGC7901细胞周期及凋亡的作用。应用Western Blot法观察SGC7901Caspase-9、Caspase-3、PARP、pERK、ERK蛋白表达。结果 TCS处理后的SGC7901出现了皱缩、变形,对SGC7901细胞的生长有明显的抑制作用,并且阻滞于S期。TCS诱导SGC7901发生凋亡,呈浓度依赖性(r=0.901,P<0.05)。Caspase-9、Caspase-3、PARP蛋白表达降低,呈浓度依赖性(r=-0.984,r=-0.991,r=-0.951,P<0.05)。并且随着TCS浓度的升高,ERK表达降低,呈药物浓度依赖性(r=-0.957,P<0.05),TCS处理(7μmol/L和14μmol/L)激活ERK,磷酸化ERK升高(P<0.05)。结论 TCS可以抑制SGC7901细胞的生长,诱导细胞凋亡,其机制与ERK信号通路有关。

Objective To observe the effect and mechanism of trichosanthin（TCS）on inducing apoptosis of human gastric cancer cell line SGC7901.Methods The effect of 0,7,14,28μmol/L TCS on SGC7901 cell was detected from the points of view of cell morphology as well as cell counting using fluorescence microscope.In addition,the role of different concentrations of TCS in SGC7901 cell cycle and apoptosis was determined using flow cytometer.Moreover,changes in expression of Caspase-9,Caspase-3,PARP,pERK,ERK in SGC7901 were observed using Western Blot.Results Shrinkage and deformation of SGC7901 cell could be observed after TCS treatment.Proliferation of SGC7901 was remarkably inhibited by TCS treatment,which was arrested in S phase.TCS treatment could induce apoptosis of SGC7901 in a concentration-dependent manner（r=0.901,P〈0.05）.The protein expression of Caspase-9,Caspase-3 and PARP were decreased in a dose-dependent manner after TCS treatment（r=-0.984,r=-0.991,r=-0.951,P〈0.05）.Expression of ERK was also decreased in a dose-dependent manner after TCS treatment（r=-0.957,P〈0.05）.Furthermore,TCS（7 and 14μmol/L）could activate ERK,which had increased the phosphorylated ERK（P〈0.05）.Conclusions TCS can inhibit the growth of gastric cancer cell SGC7901 and induce its apoptosis.The mechanism may be related to activating the ERK signaling pathway.