论文部分内容阅读
目的研究NVP-BEZ235体外对胆管癌细胞株QBC939增殖及凋亡的影响。方法在体外培养人胆管癌细胞株QBC939,通过流式细胞仪检测NVP-BEZ235对QBC939凋亡的影响;MTT法检测NVP-BEZ235作用24小时、48小时和72小时对QBC939的增殖影响;Western blot分析NVP-BEZ235作用48小时对QBC939凋亡的影响(PARP),并检测分析相关信号通路蛋白Bcl-2、Akt、p-Akt、c-FLIPL和Mcl-1表达水平的变化。结果 NVP-BEZ235能抑制QBC939的增殖,抑制作用具有时间依赖性和浓度依赖性,同时能诱使细胞发生凋亡。NVP-BEZ235导致细胞内抗凋亡蛋白Mcl-1、c-FLIPL和Bcl-2表达下调,并降低p-Akt表达。结论 NVP-BEZ235抑制Akt的磷酸化,NVP-BEZ235通过PI3K/Akt通路下调Bcl-2、Mcl-1和c-FLIPL的表达,从而诱使QBC939出现凋亡,抑制QBC939增殖。
Objective To investigate the effects of NVP-BEZ235 on proliferation and apoptosis of cholangiocarcinoma cell line QBC939 in vitro. Methods The human cholangiocarcinoma cell line QBC939 was cultured in vitro. The effect of NVP-BEZ235 on the apoptosis of QBC939 cells was detected by flow cytometry. The effect of NVP-BEZ235 on the proliferation of QBC939 cells was detected by MTT assay. The effect of NVP-BEZ235 on the apoptosis of QBC939 cells (PARP) was analyzed and the changes of the expression of Bcl-2, Akt, p-Akt, c-FLIPL and Mcl- Results NVP-BEZ235 could inhibit the proliferation of QBC939 in a time-dependent and concentration-dependent manner and induce cell apoptosis. NVP-BEZ235 resulted in the down-regulation of the expression of intracellular anti-apoptotic proteins Mcl-1, c-FLIPL and Bcl-2 and down-regulated the expression of p-Akt. Conclusions NVP-BEZ235 inhibits the phosphorylation of Akt. NVP-BEZ235 down-regulates the expressions of Bcl-2, Mcl-1 and c-FLIPL through the PI3K / Akt pathway, inducing the apoptosis of QBC939 and inhibiting the proliferation of QBC939.