NM-3对体外胃癌细胞株SGC-7901的作用和机制探讨

The Effect of NM-3 on Cells Proliferation and Apoptosis of the Human Gastric Cancer Cell SGC-7901 in vitro

目的:研究新小分子血管生成抑制剂NM-3对体外培养的胃癌SGC7901细胞的作用,并探讨NM-3对胃癌抑制作用的机理。方法:将体外培养的人胃癌细胞株SGC7901用NM-3、卡铂及生理盐水处理,观察细胞的生长规律。并在不同时间段以流式细胞仪检测细胞的凋亡率,分析细胞周期分布。结果:将药物作用后1 h,2 h,3 h,6 h,12 h,24 h,48 h,72 h 的胃癌SGC7901细胞通过流式细胞仪检测胃癌细胞早期凋亡率及凋亡峰。发现NM-3组(1 mol／L)在72h内与对照组比较细胞早期调亡率无显著差异(P>0．05);经0．1mol／L卡铂处理的细胞组早期即可诱导发生明显的凋亡,并随着时间的延长调亡率增高,呈时间依赖性,与对照组相比较,有显著差异(P<0．05)。对细胞周期分布的分析中,NM-3组(1mg／L) Sub-G1峰与对照组比较无显著差异(P>0．05)。而卡铂能使细胞周期发生相对变化,随着药物作用时间的增加,G0／G1期细胞增多,而S期及G2／M期细胞则相应减少。结论:NM-3对胃癌组织的生长抑制主要是通过作用于血管内皮细胞,减少肿瘤新生血管生成。而对体外培养的人胃癌细胞无直接诱导其凋亡的作用。

To study the action of NM3, which is a kind of angiogenesis inhibitor, on the growth and apoptosis of human gastric carcinoma cell line SGC-7901 and discuss its action mechanism Methods：Human gastric carcinoma cell line SGC-7901 was treated with NM-3, Carboplatin and NS. Cell proliferation was evaluated with MTT assay, Distributions of cell cycle and ap optosis rate were determined with flow cytometry, cell apoptosis was confirmed by morphology. Results： The inhibition effect of NM-3 was not apparent on the proliferation of SGC2-7901 compared with controls, the apoptosis rate was not statistically different （P〈0. 05）. In cell cycle analysis, NM-3 could not increase the proportion of cells in the G0/G1 phase which was an indication of early apoptosis. Conclusion：NM-3 could not induce the apoptosis of human gastric cancer cell SGC-7901 in vitro, it enhanced the sensitivity of Carboplatin on human gasric cancer cell SGC-7901 in vitro. It had no direct effect on proliferation of gastric carcinoma cells. The anticancer mechanism of NM-3 in animal model was mainly related to its antiangiogenesis action.