EGF通过激活FAK—PI3K／AKT途径促进肺癌细胞增殖

EGF Promotes the Proliferation of Lung Cancer Cell by FAK-PI3K/AKT Pathway

目的探讨在EGF处理下，FAK—PI3K／AKT途径促进A549细胞增殖的作用。方法应用MTr法检测细胞的增殖，使用Western印迹检测FAK397位点及AKT的磷酸化水平，并应用RNAi干涉技术探讨各途径间的关系。结果MTT法证明EGF可以通过PI3K／AKT途径促进A549细胞的增殖，Westem印迹检测显示EGF处理可以促进FAK397位点和AKT的磷酸化。FAKRNAi结果表明EGF通过磷酸化FAK激活PI3K／AKT途径。结论EGF可以通过激活FAK—PI3K／AKT途径促进A549细胞增殖。

Objective To investigate the role of FAK-PI3K/AKT pathway in the proliferation of A549 cells that were treated with EGF. Methods MTT test was used to assess the proliferation of A549. Western blot was applied to evaluate the phosphorylation level of FAK tyr397 and AKT. FAK RNAi was used to analyse the relationship between FAK phosphorylation and AKT phosphorylation in this pathways, Results MTT test showed that EGF enhanced the proliferation of A549, Western blot result suggested that EGF treatment increased the phosphorylation of FAK tyr397 and AKT. FAK RNAi abolished the phosphorylation of AKT that was stimulated by EGF, Conclusion FAK-PI3K/AKT pathway is involved in the proliferation of A549 that is stimulated by EGF.