期刊
ONCOGENE
卷 29, 期 9, 页码 1280-1292出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2009.428
关键词
caspase-2; survivin; NF kappa B; RIP1; tumor growth; gene expression
资金
- National Institutes of Health [CA78810, CA90917, CA118005]
One of the pivotal functions of endogenous tumor suppression is to oppose aberrant cell survival, but the molecular requirements of this process are not completely understood. Here, we show that caspase 2, a death effector with largely unknown functions, represses transcription of the survivin gene, a general regulator of cell division and cytoprotection in tumors. This pathway involves caspase 2 proteolytic cleavage of the nuclear factor kappa B (NF kappa B) activator, RIP1. In turn, loss of RIP1 abolishes transcription of NF kappa B target genes, including survivin, resulting in deregulated mitotic transitions, enhanced apoptosis and suppression of tumorigenicity in vivo. Therefore, caspase 2 functions as an endogenous inhibitor of NF kappa B-dependent cell survival and this mechanism may contribute to tumor suppression in humans. Oncogene (2010) 29, 1280-1292; doi: 10.1038/onc.2009.428; published online 23 November 2009
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据