索拉菲尼对人胃癌细胞SGC-7901增殖、凋亡和P-ERK表达的影响  

The effect of sorafenib on growth,apoptosis and P-ERK expression in human gastric cancer SGC-7901 cells

作　　者：李端永[1] 李良庆[1] 

机构地区：[1]福建医科大学第一临床医学院胃肠外科,福建福州350005

出　　处：《中国普通外科杂志》2011年第4期367-371,共5页China Journal of General Surgery

摘　　要：目的探讨多分子靶向药物索拉菲尼(sorafenib)对体外人胃癌细胞SGC-7901增殖、凋亡的影响及对癌细胞P-ERK表达的影响,并探讨其可能机制。方法以MTT法检测索拉菲尼对SGC-7901细胞的杀伤抑制作用;免疫细胞化学法检测胃癌细胞内P-ERK蛋白的表达;流式细胞仪检测胃癌细胞凋亡的变化情况。结果索拉菲尼对胃癌细胞生长增殖具有抑制作用,随药物浓度的增加作用也增强,呈剂量—时间双效应关系(P<0.05);经索拉菲尼处理的SGC-7901细胞的P-ERK表达明显下降(P<0.05);细胞凋亡率增高(P<0.05)。结论 sorafenib在体外对SGC-7901细胞具有明显的抑制作用,主要机制为抑制其P-ERK表达,从而抑制其增殖和促进凋亡。Objective To investigate the multiple molecular targeted agent,sorafenib,in human gastric cancer SGC-7901 cell proliferation,apoptosis and P-ERK expression,and explore its possible mechanism.Methods MTT method was used to detect antiproliferative ratio of sorafenib on human gastric cancer SGC-7901 cell;immunocytochemical method for detection of gastric cancer cells P-ERK protein expression;and flow cytometry to analyze gastric cancer cell apoptosis.Results Sorafenib obviously inhibited proliferation of gastric cancer cells and showed time-dose-dependent effects（P0.05）.When gastric cancer SGC-7901 cells were treated with sorafenib,immunocytochemistry showed that P-ERK expression was significantly decreased（P0.05）;flow cytometry showed that the SGC-7901 cell apoptosis rate increased（P0.05）.Conclusions Sorafenib can significantly inhibit human gastric cancer SGC-7901 cell growth in vitro;the main mechanism is the inhibition of P-ERK expression,and thereby inhibit their proliferation and promote apoptosis.

关 键 词：胃肿瘤/病理学 索拉菲尼 SGC-7901细胞 细胞增殖 细胞凋亡 P-ERK 流式细胞术 

分 类 号：R730.2[医药卫生—肿瘤]