Tumor Growth Suppression by the Coactivator p300
Tumor Growth Suppression by the Coactivator p300
复制标题
DOI：
10.1016/s1349-0079(08)80025-4
复制
发表时间：
2008
影响因子：
2.4
通讯作者：
Tamaki Suganuma;M. Ikeda
中科院分区：
文献类型：
--
作者：
Tamaki Suganuma;M. Ikeda
p300和密切相关的CREB结合蛋白（CBP）乙酰转移酶作为全球转录共激活因子发挥作用，并在广泛的生物过程中发挥重要作用，包括细胞增殖，分化和凋亡。p300/CBP在肿瘤抑制中的作用是基于以下事实提出的：这些共激活因子被病毒癌蛋白靶向，并且在某些类型的癌中已经鉴定出与第二等位基因失活相关的p300/CBP突变。然而，p300/CBP的失活导致癌变的机制尚未完全阐明。本文就p300在肿瘤抑制中的作用，特别是其与TGF-β依赖性转录反应的关系，以及p300突变对p53通路和细胞增殖的影响作一综述。
The p300 and closely related CREB-binding protein (CBP) acetyltransferases function as global transcriptional coactivators and play important roles in a broad spectrum of biological processes, including cell proliferation, differentiation, and apoptosis. The role of p300/CBP in tumor suppression has been proposed based on the fact that these coactivators are targeted by viral oncoproteins, and that mutations of p300/CBP associated with inactivation of the second allele have been identified in certain types of carcinoma. However, the mechanisms by which the inactivation of p300/CBP contributes to carcinogenesis have not been fully elucidated. In this review, we focus on the understanding of p300 function in tumor suppression, particularly with regard to its relationship with the TGF-β-dependent transcriptional response, which is important for the negative growth regulation of epithelial cells, and also discuss the effects of p300 mutation on the p53 pathway and cell proliferation.