抑制PI3K／Akt信号通路对Ephrin—A1介导的肝癌细胞运动和侵袭能力的影响

PI3K/Akt signal effects Ephrin-A1 mediated malignancy of HCC cells

目的探讨PI3K／Akt信号传导通路在Ephrin—A1介导的肝癌细胞侵袭、转移过程中的作用。方法Western blot法检测Ephrin-A1／Fc融合蛋白作用人肝癌细胞系Huh-7细胞前后丝裂原激活的蛋白激酶（MAPK）和磷脂酰肌醇3激酶（PI3K）信号分子的表达，利用LY294002特异性的阻断PI3K／Akt信号通路后，检测细胞运动能力、细胞侵袭能力的变化。结果Ephrin—A1／Fc融合蛋白作用后p-Akt磷酸化蛋白的表达与对照组比较明显上升（t=4．564，P〈0．05），PI3K／Akt信号通路可能为Ephrin—A1／EphA1作用的下游信号传导通路；LY294002明显抑制Ephrin—A1／Fc融合蛋白对Huh-7细胞中PI3K／Akt信号通路的激活，p-Akt磷酸化蛋白的含量与对照组比较明显减少（P〈0．05）；Ephrin-A1介导肝癌细胞的运动能力及侵袭能力明显受到抑制（P〈0．05）。结论PI3K／Akt信号通路在Ephrin—A1介导的肝癌细胞侵袭、转移过程中起重要的作用。

Objective To investigate the role of PI3K/Akt signal pathway in Ephrin-A1 gene mediated invasion, metastasis of Huh-7 cells. Methods Western blot was used to test the protein expression of phosphatidylinositol 3-kinase （PI3K） and mitogen- activated protein kinase （MAPK） after Huh-7 cells were treated with Ephrin-A1/Fc fusion protein. According to the protein expression, LY294002 was used to block PI3K/Akt pathway specifically, then p-Akt protein expression, mobility and invasive ability of Huh-7 cells were examined. Results In Huh-7 cells aetived by Ephrin-A1/Fe fusion protein, p-Akt expression was higher than that in control group（ t = 4. 564, P 〈 0. 05 ） , but there was no difference of p-p38MAPK expression between Ephrin-A1/Fc fusion protein group and IgG/Fc fusion protein group（ P 〉 0. 05 ）. PI3 K/Akt pathway was specifically blocked by LY294002, the p-Akt protein expression decreased in Huh-7 cells, and the mobility and invasive ability mediated by Ephrin-A1 in Huh-7 cells decreased （ P 〈 0.05 ）. Conclusions PI3K/Akt pathway effects an important role in mobility and invasive ability of Huh- 7 cells mediated by Ephrin-Al.