亚砷酸钠对人胃癌细胞株SGC-7901作用机制的研究  

The study of antitumor mechanism of sodium arsenite on gastric carcinoma cell line SGC-7901 in vitro

作　　者：赵文韬[1] 王严庆[1] 汤为学[2] 

机构地区：[1]重庆医科大学附属第一医院普外科 [2]重庆医科大学病理生理教研室

出　　处：《肿瘤研究与临床》2006年第4期220-222,230,共4页Cancer Research and Clinic

摘　　要：目的探讨亚砷酸钠对人胃癌细胞株SGC-7901生物学行为的影响及其作用机制。方法采用MTT法、光镜、电镜、流式细胞仪检测和免疫细胞化学方法研究亚砷酸钠对人胃癌细胞株SGC-7901生物学行为的影响。结果不同浓度(2.50～40.00μmol/L)的亚砷酸钠均能抑制SGC-7901细胞生长,且具有浓度和时间依赖性,其作用72h的中效浓度为8.69μmol/L。流式细胞仪检测发现亚砷酸钠作用48h,72h后,SGC-7901细胞出现G2/M期阻滞。形态学观察显示亚砷酸钠作用72h后,细胞出现典型的凋亡和坏死形态学改变。免疫细胞化学法发现亚砷酸钠能显著上调细胞Caspase-3蛋白的表达。结论亚砷酸钠对SGC-7901细胞的生长有明显的抑制作用,并可诱导细胞周期阻滞及细胞凋亡和坏死,其机制可能与其抑制ROS的清除,上调Caspase-3蛋白的表达有关。Objective To investigate the antitumor mechanism of sodium arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MIT assay, light microscopy, electron microscopy, flow cytometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic behavior of SGC-7901 ceils. Results Sodium arsenite （2.50 - 40.00μmol/L） could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration（ICS0） was 8.69 μmol/L after 72 hours＇ treatment. SGC-7901 ceils were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 ceils presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 cells, induce cell cycle arrest and apoptosis and necrosis of the cells, its mechanism is possibly associated with inhibition of elimination of ROS and the up-regulated expression of Caspase-3 protein.

关 键 词：亚砷酸钠 人胃癌细胞株SGC-7901 

分 类 号：R735.2[医药卫生—肿瘤]