阻断PI3K/AKT通路抑制棕榈酸诱导的肝癌细胞凋亡

Inhibition of the PI3K/AKT pathway suppresses palmitic acid-induced hepatocellular carcinoma cell apoptosis

目的:探讨三磷酸酰肌醇蛋白激酶(PI3K)信号通路与棕榈酸(palmitic acid,PA)诱导肝癌细胞凋亡的关系。方法:培养人肝癌细胞系PLC、SMMC-7721及LM3,经PA及三磷酸酰肌醇蛋白激酶(Phosphotidylinsitol-3-Kinase,PI3K)抑制剂LY294002处理细胞后,利用倒置相差显微镜观察细胞形态;通过Western blotting分析阻断PI3K/AKT信号通路与PA诱导PLC、SMMC-7721及LM3细胞凋亡之间的关系。结果 :PA处理明显诱导PLC、SMMC-7721及LM3细胞发生凋亡;阻断PI3K/AKT信号通路抑制了PA对上述肝癌细胞凋亡的诱导。结论:阻断PI3K/AKT信号通路可抑制PA诱导的肝癌细胞凋亡。

Objective： To investigate the link between PI3K/AKT pathway and palmitic acid（PA）-induced hepatocellular carcinoma cell apoptosis. Methods： The role of PI3 K inhibitor LY294002 in PA-induced apoptosis of hepatocellular carcinoma cells, including PLC, SMMC-7721 and LM3, was investigated. Inverted phase contrast microscope was used to observe cell morphology,Western blot and flow cytometry were used to investigate the relationship between the blockage of PI3K/AKT pathway and apoptosis of PLC, LM3 and SMMC-7721 cells.Results： PA treatment resulted in apoptosis of PLC, SMMC-7721 and LM3 hepatocellular carcinoma cells. The PI3K/AKT pathway blockage inhibited the apoptosis of hepatocellular carcinoma cells mediated by PA.Conclusion： Blocking the PI3K/AKT pathway can suppress PA-induced hepatocellular carcinoma cell apoptosis.