中文摘要：

目的研究FAK调节肺癌细胞系A549抗失巢凋亡的功能和信号通路。方法应用光镜观察，Hoechst33342染核、电镜、Western印迹、RNA干涉技术、P13K的抑制剂，对FAK调节肺癌细胞A549抗失巢凋亡的功能和信号通路进行研究。结果发现肺癌细胞系A549具有抗失巢凋亡的能力；A549细胞悬浮培养时，FAKtyr-397／861／925的活性随时间的延长逐渐增加后降低，磷酸化的P13K和AKT表现出与其一致的活性变化；通过RNA干涉实验发现干涉组比对照组细胞出现明显的凋亡现象，同时P13K／AKT的磷酸化水平下降；P13K的抑制剂组比对照组出现更多的凋亡细胞。结论FAK在肺癌细胞A549抗失巢凋亡中发挥了重要作用，其抗失巢凋亡的机制是通过激活下游P13K／AKT通路来实现的。

英文摘要：

Objective To study the function and signaling pathway on FAK resisting anoikis in lung cancer cell, A549. Methods Light microscope, Hoechst33342 stain, electron microscope, western blot, siRNA-FAK technique and the inhibitor of PI3K were employed to study the activity of FAK, PI3K and AKT in resisting anoikis. Results Lung cancer cell A549 could resist anoikis; When the cells were cultured under suspended conditions, the activity of FAKtyr-397/861/925 increased gradually and decreased at last, and the ／ level of phosphorylated PI3K and AKT showed the same trend with FAK; Compared with the control group, more apoptotic cells were found in siRNA-FAK group, and meanwhile, phosphorylated PI3K and AKT decreased. More apoptotic cells were found in ly294002 treated group than control. Conclusion FAK plays an important role in resisting anoikis of lung cancer cell, A549, which is caused by activity of PI3K/AKT kinases that are stimulated by FAK.