三氧化二砷诱导胃癌细胞凋亡及相关蛋白Cpp32激活的初步研究

STUDIES ON ARSENIC TRIOXIDE INDUCING APOPTOSIS AND THE ACTIVATION OF CPP32 IN GASTRIC CARCINOMA CELL

目的 :探讨三氧化二砷 (As2 O3)的抑胃癌作用及其可能的分子机制。方法 :采用MTT、HE和westernblotting的方法观察三氧化二砷对体外胃癌细胞恶性增殖的抑制及其对相关蛋白Cpp3 2的影响。 结果 :As2 O3对癌细胞的抑制有明显的时间和剂量依赖性 ,2 5 μM的As2 O3作用胃癌细胞 48h呈现出典型的细胞凋亡形态学特征 ;同时其相关蛋白Cpp3 2被裂解激活 ,并随As2 O3作用剂量增加而含量减少。结论 :一定量的As2 O3能诱导胃癌细胞凋亡 ,抑制胃癌细胞的恶性生长 ,且天胱蛋白Cpp3 2可能参与介导这一凋亡效应。

Objectives:To determine the effect and the possible molecular mechanism of arsenic trioxide (As 2O 3) inhibiting human gastric carcinoma cell.Methods:With MTT?HE and Western blotting methods,the effect of As 2O 3 on the inhibiting of growth and activity of Cpp32 in cancer cell was eraluated.Results:The effect of As 2O 3 on cancer cell depression was depending on the time and concentration conspiciously;48 after 2 5mol/L As 2O 3 treated gastric carcinoma cell in vitro and some typical features of apoptosis were presented;meanwhile,the analysis of blotting showed that Cpp32 was splitted and activated,which reduced significantly when the concentration of As 2O 3 increased continuously.Conclusion:Toxic agent As 2O 3 in effective dose can induce apoptosis of gastric carcinoma cell and inhibit its abnormal proliferation,which might be related to activity of Cpp32.