APAF-1 signaling in human melanoma

被引:24
作者
Anichini, Andrea [1 ]
Mortarini, Roberta [1 ]
Sensi, Marialuisa [1 ]
Zanon, Marina [1 ]
机构
[1] Ist Nazl Studio & Cura Tumori, Dept Expt Oncol, Unit Human Tumor Immunobiol, I-20133 Milan, Italy
关键词
APAF-1; apoptosis; melanoma;
D O I
10.1016/j.canlet.2005.06.034
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Acquired resistance to mechanisms of programmed cell death is one of the hallmarks of cancer. Human melanoma, in advanced stage, is hardly curable, due to development of several strategies that impair apoptosis induced by the death receptor and the mitochondrial pathways of apoptosis. Among these apoptosis escape strategies, one is based on inactivation of prop 1 apoptotic factors such as Apoptotic Protease Activating Factor-1 (APAF-1). APAF-1 couples cytochrome c release from the mitochondria to caspase-9 activation and has been considered a central adaptor in the intrinsic pathway of programmed cell death. Inactivation of APAF-1 in human melanoma may impair the mitochondrial pathway of apoptosis induced by chemotherapeutic drugs that activate the p53 pathway, thus contributing to the development of chemoresistance. In-vivo, loss of expression of APAF-1 is associated with tumor progression, suggesting that APAF-1 inactivation may provide a selective survival advantage to neoplastic cells. However, recent results have indicated the existence of APAF-1-independent pathways of caspase activation and apoptosis in normal and neoplastic cells. Moreover, it has been found that expression of APAF-1 is not necessary for the apoptotic response of melanoma cells to different pro-apoptotic drugs. The emerging picture from results obtained in melanoma and other human tumors is that the relevance of the APAF-1 pathway in programmed cell death is cell-context-dependent and related to the specificity of the pro-apoptotic-stimuli. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:168 / 179
页数:12
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