PI3K/AKT/mTOR信号通路在诱导胶质瘤细胞凋亡中的作用

Curcumol induces apoptosis of U87 cells via the PI3K/AKT/mTOR pathway

目的:观察莪术醇对胶质瘤U87细胞凋亡的诱导作用及其作用机制。方法:采用MTT法检测细胞增殖,Annexin V/PI双染法检测细胞凋亡,Western blot检测蛋白表达及磷酸化水平,采用m TOR的特异性抑制剂雷帕霉素探讨莪术醇的作用靶点。结果:莪术醇对U87细胞的增殖抑制作用呈浓度和时间依赖性,莪术醇显著诱导了U87细胞凋亡。莪术醇和雷帕霉素均下调了PI3K,p-AKT,pm TOR,e IF4E蛋白的表达,雷帕霉素部分废除了莪术醇的药理作用。结论:莪术醇诱导U87细胞凋亡的分子机制涉及PI3K/AKT/m TOR信号通路。

Objective： To investigate the underlying mechanisms of curcumol（ Cur）-induced apoptosis in human glioma U87 cells. Methods： The cell viability was assessed by MTT assay. The cell apoptosis rate was analyzed by Annexin V / PI staining. The expression level of PI3 K,p-AKT,p-m TOR,and e IF4 E proteins was detected by Western blotting. Results： Cur significantly inhibited proliferation of U87 cells in a time- and concentration-dependent manner,and induced apoptosis. Cur down-regulated the expression of p-AKT,p-m TOR,and e IF4 E proteins. Conclusion： The inhibition of the growth of human U87 neuroblastoma cells by Cur may be associated suppression of the PI3 K / Akt / m TOR signaling pathway.