磷脂酰肌醇3激酶抑制剂BKM120抑制U251神经胶质瘤细胞增殖并促进其凋亡

Phosphatidylinositide 3-kinase inhibitor BKM120 suppresses proliferation and promotes apoptosis of U251 glioblastoma cells

目的探讨磷脂酰肌醇3激酶(PI3K)抑制剂BKM120对U251神经胶质瘤细胞凋亡的诱导作用。方法用(1、5、20)μmol/L BKM120处理U251细胞48 h后,采用CCK-8法检测BKM120对U251细胞增殖的影响,用异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)双染法标记结合流式细胞术检测细胞凋亡,Western blot法检测Bax和Bcl-2的蛋白水平。结果 BKM120能抑制U251神经胶质瘤细胞的增殖并呈一定的浓度依赖性,最大抑制率为78.3%。BKM120处理可引起U251细胞凋亡。Western blot结果显示BKM120处理可引起Bax蛋白水平增加,同时Bcl-2蛋白水平降低。结论BKM120能抑制U251细胞的增殖并促进细胞凋亡。

Objective To investigate the effect of phosphatidylinositide 3-kinase （P13K） inhibitor BKM120 on the proliferation and apoptosis of human glioma U251 cells. Methods U251 cells were treated with different concentrations of BKMI20 （final concentrations were 1, .5, 20 μmol/L） for 48 hours. The effect of BKMI20 on cell proliferation was detected by CCK-8 assay. The apoptosis was detected by annexin V-FITC/PI staining. The protein expressions of Bax and Bcl-2 were detected by Western blotting. Results CCK-8 assay showed that BKM120 inhibited U251 proliferation in a concentration- dependent manner and the maximum inhibitory rate was 78.3%. Flow cytometry showed that BKM120 induced cell aopotosis in a concentration-dependent manner. Western blotting revealed that the expression of Bax was elevated by BKM120, but the expression of Bcl-2 had a reverse trend. Conclusion BKM120 can inhibit the proliferation and induce the apoptosis of U251 cells.