DAPT抑制胃癌BGC-823细胞增殖的体外实验研究

目的探讨Notch信号通路抑制剂氮-氮-（3,5-二氟苯乙酰）-L-丙氨酰]-S-苯基甘氨酸丁酯（DAPT）对胃癌细胞系BGC-823增值率的影响及其机制。方法体外培养BGC-823细胞,利用MTT检测DAPT引起的BGC-823细胞增值率的变化以及Western Blotting检测DAPT对凋亡相关蛋白caspase-3、Cytochrome C、Bcl-2和Bax表达水平的影响。结果与对照组相比,不同浓度DAPT可以引起明显的BGC细胞增值率的下降,同时凋亡相关蛋白caspase-3表达水平明显上升,线粒体凋亡相关蛋白Bax/Bcl-2比率、Cytochrome C表达水平明显升高。结论 Notch信号通路抑制剂DAPT可以通过线粒体凋亡通路诱导BGC-823细胞凋亡,抑制细胞增殖。

Study of Notch signaling inhibitor DAPT on cell proliferation of stomach cancer BGC-823 cells

Objective To investigate the effect of Notch signaling inhibitor N-（ N-（3,5-difluorophenacetyl）-1-alanyl）-S-phenylglycine t-butyl ester（DAPT） on cell proliferation of stomach cancer BGC-823 cells. Methods MTT assay was employed to examine the growth suppression of the cells. Western Blotting was used to detect the expressions of Caspase-3 、Bax/Bcl-2 and Cytochrome C. Results MTT assay showed that vary dosages of DAPT decreased the growth rate of BGC-823 cells. DAPT could increase the expressions of Caspase-3 、Bax/Bcl-2 and Cytochrome C. Conclusion Notch signaling inhibitor DAPT could induce the apoptosis of stomach cancer BGC-823 cells through mitochondrial pathway and decrease the proliferation rate.