Caspase-mediated programmed cell death pathways as potential therapeutic targets in cancer

被引：120

作者：

Wen, X. ^{[1
,2
]}

Lin, Z. -Q. ^{[1
,2
]}

Liu, B. ^{[1
,2
]}

Wei, Y. -Q. ^{[1
,2
]}

机构：

[1] Sichuan Univ, State Key Lab Biotherapy, Chengdu 610041, Peoples R China

[2] Sichuan Univ, Ctr Canc, W China Hosp, W China Med Sch, Chengdu 610041, Peoples R China

来源：

CELL PROLIFERATION | 2012年 / 45卷 / 03期

关键词：

NF-KAPPA-B; CYTOCHROME-C; AUTOPHAGIC PATHWAYS; IN-VIVO; APOPTOSIS; ACTIVATION; CLEAVAGE; INHIBITION; PROTEINS; CYTOTOXICITY;

D O I：

10.1111/j.1365-2184.2012.00814.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The caspase family is well characterized as playing a crucial role in modulation of programmed cell death (PCD), which is a genetically regulated, evolutionarily conserved process with numerous links to many human diseases, most notably cancer. In this review, we focus on summarizing the intricate relationships between some members of the caspase family and their key apoptotic mediators, involving tumour necrosis factor receptors, the Bcl-2 family, cytochrome c, Apaf-1 and IAPs in cancer initiation and progression. We elucidate new emerging types of cross-talk between several caspases and autophagy-related genes (Atgs) in cancer. Moreover, we focus on presenting several PCD-modulating agents that may target caspases-3, -8 and -9, and their substrates PARP-1 and Beclin-1, which may help us harness caspase-modulated PCD pathways for future drug discovery.

引用

页码：217 / 224

页数：8

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