Desipramine induces apoptotic cell death through nonmitochondrial and mitochondrial pathways in different types of human colon carcinoma cells
Desipramine induces apoptotic cell death through nonmitochondrial and mitochondrial pathways in different types of human colon carcinoma cells
复制标题
DOI：
10.1159/000111144
复制
发表时间：
2008-01-01
期刊：
影响因子：
3.1
通讯作者：
Morita, Kyoji
中科院分区：
文献类型：
--
作者：
Arimochi, Hideki;Morita, Kyoji
观察地西帕明对人结肠癌HT29和HCT116细胞的细胞毒作用。地西帕明对HT29细胞的活性降低呈浓度依赖性，但当浓度达到50 μ mol/l时，对HCT116细胞的活性没有明显影响，在50 μ mol/l时，HT29细胞的活性降低约60%。尽管它们的敏感性不同，地西帕明对两者都造成非氧化性凋亡损伤。与HT29细胞相反，地西帕明可能通过干扰线粒体功能导致HCT116细胞凋亡。这些结果表明，地西帕明可能通过非线粒体或线粒体途径引起不同类型的人结肠癌细胞的非氧化性凋亡损伤，这可能导致这些肿瘤细胞对该药物的不同敏感性。版权所有2008 S. Karger AG，巴塞尔
Cytotoxic effects of desipramine on human colon carcinoma HT29 and HCT116 cells were examined. Desipramine reduced the viability of HT29 cells in a concentration-dependent manner, but failed to cause any significant change in the viability of HCT116 cells by the concentration up to 50 mu mol/l, at which an approximately 60% reduction of the viability of HT29 cells was observed. Despite their different sensitivities, desipramine caused the nonoxidative apoptotic damage to both of them. In contrast to HT29 cells, desipramine might cause the apoptotic death of HCT116 cells through the disturbance of mitochondrial function. These results suggest that desipramine may cause the nonoxidative apoptotic damage to different types of human colon carcinoma cells through either a nonmitochondrial or a mitochondrial pathway, which may confer the different sensitivities to this drug on these tumor cells. Copyright (C) 2008 S. Karger AG, Basel.