NAD+激酶
癌变
西妥因1
组蛋白
生物
烟酰胺腺嘌呤二核苷酸
乙酰化
组蛋白脱乙酰基酶
癌症研究
抑制器
表观遗传学
细胞生物学
癌症
转录调控
基因
遗传学
基因表达
生物化学
下调和上调
酶
作者
Jiayi Yin,Xin-Tong Lu,Meng-Ling Hou,Ting Cao,Zhen Tian
标识
DOI:10.1016/j.bcp.2023.115543
摘要
Sirtuin1 (SIRT1) is a conserved nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase that plays key roles in a range of cellular events, including the maintenance of genome stability, gene regulation, cell proliferation, and apoptosis. P53 is one of the most studied tumor suppressors and the first identified non-histone target of SIRT1. SIRT1 deacetylates p53 in a NAD+-dependent manner and inhibits its transcriptional activity, thus exerting action on a series of pathways related to tissue homeostasis and various pathological states. The SIRT1-p53 axis is thought to play a central role in tumorigenesis. Although SIRT1 was initially identified as a tumor promoter, evidence now indicates that SIRT1 may also act as a tumor suppressor. This seemingly contradictory evidence indicates that the functionality of SIRT1 may be dictated by different cell types and intracellular localization patterns. In this review, we summarize recent evidence relating to the interactions between SIRT1 and p53 and discuss the relative roles of these two molecules with regards to cancer-associated cellular events. We also provide an overview of current knowledge of SIRT1-p53 signaling in tumorigenesis. Given the vital role of the SIRT1-p53 pathway, targeting this axis may provide promising strategies for the treatment of cancer.
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