三氧化二砷启动人食管癌细胞凋亡机制研究

目的探讨三氧化二砷诱导白血病及实体瘤细胞凋亡的机制。方法以三氧化二砷敏感和不敏感人食管癌细胞株为模型，运用RT-PCR和流式细胞术检测三氧化二砷处理的这两类细胞Fas／FasL表达的改变；同时利用荧光探针检测线粒体功能变化。结果两类细胞有同等水平Fas表达，但均未检测出FasL；三氧化二砷既不能上调Fas也不能诱导FasL表达，但破坏线粒体跨膜电势和氧化-还原系统。结论三氧化二砷诱导人食管癌细胞凋亡不依赖Fas／FasL的启动，而直接作用于线粒体，活化Caspase-3导致凋亡。

Study on the Mechanism of As2O3-induced Apoptosis of Human Esophageal Carcinoma Cell Lines

Objective To investigate the mechanism of As2O3-induced apoptosis of human essophageal carcinoma cells. Methods The expression of Fas/FasL and the changes of mitsochondrial function were assayed in As2O3-sensitive and AS2O3-resistant human esophageal carcinoma cell lines by means of RT-PCR and flow cytometry. Results 1.The expression of Fas was not different between the above two cell lines. The expression of FasL was undetectable in both. 2. As2O3s neither elevated Fas expression nor triggered FasL expression. However, it could disrupt not only the mitochondrial transmembrane potential (in) but also its redox state (indicated by the decrease in GSH and the increase in reactive oxygen species). Conclusion Apoptosis of human esophageal carcinoma cells induced by As2O3s is Fas/FasL independent. As2O3 affects the mitochondria directly, resulting in apoptosis by activation of caspase-3(CPP32).