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目的研究蛋白酶体抑制剂MG132对胃癌细胞系AGS和SNU484细胞成活率和凋亡情况的影响及其可能的分子机制。方法蛋白酶体抑制剂MG132(1μM,10μM)处理胃癌细胞系AGS和SNU484。利用MTT法检测细胞生长状态,采用流式细胞仪测定细胞凋亡情况,利用Western blot法检测肿瘤抑制基因SMAD4蛋白表达水平。结果MG132能够以时间和剂量依赖的方式抑制AGS和SNU484的细胞增殖,且AGS对MG132的敏感性要高于SNU484细胞。MG132呈剂量依赖的方式诱导AGS和SNU484细胞凋亡。探讨相关分子机制发现MG132能够上调SMAD4蛋白的表达水平。结论用MG132处理胃癌细胞可引起细胞增殖抑制,其可能的分子机制为上调肿瘤抑制基因SMAD4的表达。蛋白酶体抑制剂可能会成为一类新的抗胃癌的药物。
Objective To study the effect of proteasome inhibitor MG132 on the survival rate and apoptosis of gastric cancer cell lines AGS and SNU484 and its possible molecular mechanism. Methods Proteasome inhibitor MG132 (1μM, 10μM) treated gastric cancer cell lines AGS and SNU484. Cell growth status was detected by MTT assay. Cell apoptosis was measured by flow cytometry. The expression of SMAD4 protein was detected by Western blot. Results MG132 inhibited cell proliferation of AGS and SNU484 in a time-and dose-dependent manner, and the sensitivity of AGS to MG132 was higher than that of SNU484 cells. MG132 induced AGS and SNU484 cell apoptosis in a dose-dependent manner. Explore the relevant molecular mechanism found that MG132 can up-regulate the expression of SMAD4 protein. Conclusion MG132 treatment of gastric cancer cells can cause cell proliferation inhibition, the possible molecular mechanism is up-regulation of tumor suppressor gene SMAD4 expression. Proteasome inhibitors may become a new class of anti-cancer drugs.