CAJ | 학술논문

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。
목적：사용소분자억제물LY294002화PD98059분별억제린지선기순-3격매（ PI3K）통로화유사분렬활화단백격매（MAPK）통로적신호전도，급여이도소양생장인자-1（IGF-1）자격，검측유선암세포적증식화천이능력적변화。방법사용CCK-8법화체외천이실험분별검측IGF-1간예하세포적증식능력，병이신호통로억제제처리후세포작위대조조，동양사용CCK-8법화체외천이실험검측기증식능력。결과 IGF-1간예제2～4천，불동농도IGF-1（20，50，100mg/L）균현저촉진MDA-MB-231세포증식，여대조조비교，차이유통계학의의（P＜0．05）；당IGF-1농도위50mg/L시촉진작용최명현；사용LY294002（25μM）혹PD98059（50μM）분별조단PI3K통로화MAPK통로후，불부억제MDA-MB-231세포기출수평적증식，이차억제IGF-1자격하적세포증식능력，여DMSO대조조비교，차이유통계학의의（P＜0．01）；재불동농도IGF-1（20，50，100mg/L）작용하，MDA-MB-231세포천이능력균증강，여대조조비교，차이유통계학의의（ P＜0．01）。결론 IGF-1간예후MDA-MB-231세포적증식화천이능력명현증강，PI3K통로화MAPK통로균삼여료IGF-1촉진유선암세포증식화천이적신호전도。
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 .