Rack1敲低促进TGF-β诱导的A549细胞的上皮-间充质转化  

Rack1 knockdown promotes epithelial to mesenchymal transition induced by TGF-β in A549 cells

作　　者：梁瑞[1,2] 张继帅[2] 叶辉[2] 杨晓[2] 漆永梅[1] 

机构地区：[1]兰州大学生命科学学院,兰州730000 [2]军事医学科学院生物工程研究所,北京100071

出　　处：《军事医学》2012年第1期27-30,共4页Military Medical Sciences

基　　金：国家自然科学基金面上项目资助(81172220)

摘　　要：目的研究Rack1分子在TGF-β诱导A549细胞发生上皮-间充质转化(epithelial to mesenchymal transition,EMT)过程中的功能。方法制备携带不同Rack1干涉序列的慢病毒颗粒,并感染A549细胞建立稳定细胞系。选取敲低效率较高的细胞系,利用MTS、细胞划痕、免疫印迹等技术检测Rack1敲低后细胞的增殖、TGF-β诱导的迁移及相关分子表达水平的改变。结果获得了Rack1稳定敲低的细胞系,Rack1敲低后细胞增殖减慢,TGF-β诱导的迁移加快,钙黏蛋白E(E-cadherin)下调和胞外信号调节激酶(extracellular regulated protein kinases,ERK)磷酸化水平升高。结论 Rack1分子敲低促进EMT的发生。Objective To investigate the role of Rack1 in TGF-β induced epithelial to mesenchymal transition（EMT） in A549 cells.Methods A549 cells were infected with lentivirus containing different shRNA for Rack1 to get Rack1 knockdown cells.The cellular proliferation,migration capacity and related molecular changes were observed with MTS assay,wound healing assay and Western blot,respectively.Results We obtained cell lines with lower Rack1 expression.After Rack1 knockdown,cell proliferation was inhibited,and cell migration induced by TGF-β was promoted.The expression of E-cadherin was downregulated and the phosphorylation of ERK was upregulated due to the knockdown of Rack1.Conclusion The knockdown of Rack1 promotes EMT in A549 cells.

关 键 词：RACK1 转化生长因子Β 上皮-间充质转化 细胞外信号调节激酶 

分 类 号：R363[医药卫生—病理学]