摘要
目的:使用小分子抑制物LY294002和PD98059分别抑制磷脂酰肌醇-3激酶( PI3K)通路和有丝分裂活化蛋白激酶(MAPK)通路的信号转导,给予胰岛素样生长因子-1(IGF-1)刺激,检测乳腺癌细胞的增殖和迁移能力的变化。方法使用CCK-8法和体外迁移实验分别检测IGF-1干预下细胞的增殖能力,并以信号通路抑制剂处理后细胞作为对照组,同样使用CCK-8法和体外迁移实验检测其增殖能力。结果 IGF-1干预第2~4天,不同浓度IGF-1(20,50,100mg/L)均显著促进MDA-MB-231细胞增殖,与对照组比较,差异有统计学意义(P<0.05);当IGF-1浓度为50mg/L时促进作用最明显;使用LY294002(25μM)或PD98059(50μM)分别阻断PI3K通路和MAPK通路后,不仅抑制MDA-MB-231细胞基础水平的增殖,而且抑制IGF-1刺激下的细胞增殖能力,与DMSO对照组比较,差异有统计学意义(P<0.01);在不同浓度IGF-1(20,50,100mg/L)作用下,MDA-MB-231细胞迁移能力均增强,与对照组比较,差异有统计学意义( P<0.01)。结论 IGF-1干预后MDA-MB-231细胞的增殖和迁移能力明显增强,PI3K通路和MAPK通路均参与了IGF-1促进乳腺癌细胞增殖和迁移的信号转导。
Objective To investigate the effects of insulin-like growth factor receptor(IGF-1R) silencing on the role of phosphatidylinositol 3-kinase ( PI3K) and mitogen-activated protein kinase ( MAPK) pathway in insulin-like growth factor ( IGF)-1 induced cell growth and migration .Methods Protein kinase inhibitors LY294002 and PD98059 were used to inhibit PI3K and MAPK pathway in vitro respectively ,and cell growth and migration induced by IGF-1 were measured.Results IGF-1R shRNA effectively inhibited proliferation and migration capacity of MDA-MB-231 cells when compared to control shRNA group .Both LY294002 and PD98059 significantly reduced the cell growth and migration in-duced by IGF-1.Conclusion PI3K and MAPK pathways play an important part in cell growth and migration induced by IGF-1 .
出处
《潍坊医学院学报》
2014年第3期195-198,共4页
Acta Academiae Medicinae Weifang