沉默IGF1R表达对胃癌细胞侵袭与迁移能力的影响及机制  

Effect of silencing IGF1R expression on invasion and migration abilities of gastric cancer cells and its mechanism

作　　者：罗玉政[1] 陈波[2] 李红樱[1] 

机构地区：[1]重庆市第九人民医院普外科,重庆400700 [2]重庆医科大学北碚附属医院普外科,重庆400700

出　　处：《中国临床研究》2018年第2期163-166,共4页Chinese Journal of Clinical Research

摘　　要：目的探讨胰岛素样生长因子1受体(IGF1R)表达量降低对胃癌细胞侵袭、迁移能力的影响及其作用机制。方法体外培养胃癌GC9811-P细胞,取对数生长期细胞,采用RNA干扰技术进行GC9811-P细胞转染。干扰组细胞转染靶向IGF1R的小干扰RNA(IGF1-siRNA);阴性组细胞转染siRNA-NC;对照组细胞不做任何处理。Transwell法检测细胞的迁移、侵袭能力,Western Blot检测转染细胞中IGF1R、丝氨酸/苏氨酸蛋白激酶(AKT)、磷酸化AKT(p-AKT)、磷脂酰肌醇-3激酶(PI3K)、磷酸化PI3K(p-PI3K)蛋白的相对表达水平。结果干扰组细胞中IGF1R蛋白的相对表达水平显著低于对照组和阴性组(P均<0.05)。干扰组细胞的迁移、侵袭数目显著低于对照组和阴性组(P均<0.05)。对照组、阴性组、干扰组细胞中AKT、PI3K蛋白的表达水平无显著差异(P均>0.05)。干扰组细胞中p-AKT、p-PI3K蛋白的表达水平较对照组和阴性组降低,差异有统计学意义(P均<0.05)。结论沉默IGF1R的表达可以降低胃癌细胞的侵袭、迁移能力,其作用机制可能是通过影响经典PI3K/AKT信号通路发挥作用。Objective To investigate the effect of lowering insulin-like growth factor 1 receptor（ IGF1 R） expression on invasion and migration abilities of gastric cancer cells and its mechanism. Methods The gastric cancer GC9811-P cells were cultured in vitro,and logarithmic phase cells were used for the transfection of GC9811-P cells by RNA interference technique. The cells in interfering group were transferred by small interference RNA targeting IG1 R（ IGF1-siRNA）. The cells in negative group were transferred by siRNA-NC. No any treatment was given for the cells in the control group.Transwell test was used to detect cell invasion and migration abilities. Western Blot method was used to detect the relative expression levels of IGF1 R,serine/threonine protein kinase（ AKT）,phosphorylated AKT（ p-AKT）,phosphoinositide3-kinase（ PI3 K） andphosphorylated PI3 K（ p-PI3 K） proteins in transferred cells. Results The relative expression level of IGF1 R protein in cells in interfering group was significantly lower than those in cells of negative group and control group（ all P〈0. 05）. The number of cells of invasion and migration in interfering group was significantly lower than those in cells of negative group and control group（ all P〈0. 05）. There were no significant differences in the expression levels of AKT and PI3 K proteins among three groups（ all P〉0. 05）. The relative expression levels of p-AKT and p-PI3 K proteins in cells of interfering group were significant lower than those in cells of negative group and control group（ all P〈0. 05）.Conclusion Silencing IGF1 R expression can decrease the invasion and migration abilities of gastric cancer cells,and the mechanism may be through the classic PI3 K/AKT signaling pathway.

关 键 词：胰岛素样生长因子1受体 胃癌 PI3K/AKT信号通路 侵袭 迁移 

分 类 号：R735.2[医药卫生—肿瘤]