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目的:探讨PI3K/Akt信号转导通路在滋养细胞侵蚀能力中的调控机制。方法:体外培养滋养细胞系。应用Western blot法检测表皮生长因子(EGF)刺激EVT后Akt、磷酸化Akt及MMP9表达的变化。应用细胞侵蚀小室检测滋养细胞的侵蚀能力。使用PI3K选择性抑制剂LY294002处理细胞,检测以上各项结果的变化。结果:①随EGF浓度增高,滋养细胞的Akt表达无明显变化,磷酸化Akt表达升高,MMP9表达升高;②EGF能够显著促进滋养细胞的侵蚀运动能力;③PI3K抑制剂LY294002明显逆转EGF对EVT侵蚀力的促进效应。结论:表皮生长因子可以活化滋养细胞的PI3K/Akt信号通路,进而促进细胞侵蚀,使用PI3K抑制剂LY294002,上述作用被抑制。
AIM: To investigate the regulatory mechanism of PI3K / Akt signal transduction pathway in trophoblast cells. Methods: In vitro cultured trophoblast cells. Western blot was used to detect the changes of Akt, phosphorylated Akt and MMP9 after epidermal growth factor (EGF) stimulation. Application of cell erosion chamber detection of trophoblast erosion. Cells were treated with the PI3K selective inhibitor LY294002 and the changes in the above results were examined. Results: (1) With the increase of EGF concentration, there was no significant change of Akt expression in trophoblast cells, the phosphorylation of Akt increased and the expression of MMP9 increased; ②EGF could significantly promote the motility of trophoblast cells; ③ PI3K inhibitor LY294002 reversed the effect of EGF on EVT The promotion effect of force. Conclusion: Epidermal growth factor can activate the PI3K / Akt signaling pathway of trophoblast and further promote cell erosion. The PI3K inhibitor LY294002 can inhibit the above-mentioned effects.