生物
细胞凋亡
抑制器
癌变
转录因子
程序性细胞死亡
癌症研究
抑癌基因
细胞生物学
癌症
遗传学
基因
作者
Jordan S. Fridman,Scott W. Lowe
出处
期刊:Oncogene
[Springer Nature]
日期:2003-12-08
卷期号:22 (56): 9030-9040
被引量:1345
标识
DOI:10.1038/sj.onc.1207116
摘要
The p53 tumor suppressor acts to integrate multiple stress signals into a series of diverse antiproliferative responses. One of the most important p53 functions is its ability to activate apoptosis, and disruption of this process can promote tumor progression and chemoresistance. p53 apparently promotes apoptosis through transcription-dependent and -independent mechanisms that act in concert to ensure that the cell death program proceeds efficiently. Moreover, the apoptotic activity of p53 is tightly controlled, and is influenced by a series of quantitative and qualitative events that influence the outcome of p53 activation. Interestingly, other p53 family members can also promote apoptosis, either in parallel or in concert with p53. Although incomplete, our current understanding of p53 illustrates how apoptosis can be integrated into a larger tumor suppressor network controlled by different signals, environmental factors, and cell type. Understanding this network in more detail will provide insights into cancer and other diseases, and will identify strategies to improve their therapeutic treatment.
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