锡尔图因
癌变
调节器
癌症研究
西妥因1
肝细胞癌
基因沉默
生物
烟酰胺腺嘌呤二核苷酸
NAD+激酶
癌症
转移
乙酰化
组蛋白脱乙酰基酶
组蛋白
遗传学
下调和上调
生物化学
基因
酶
作者
Yuting Wu,Xiao‐Ming Meng,Cheng Zhi Huang,Jun Li
出处
期刊:Tumor Biology
[SAGE]
日期:2015-04-29
卷期号:36 (6): 4063-4074
被引量:32
标识
DOI:10.1007/s13277-015-3488-x
摘要
Hepatocellular carcinoma (HCC) is one of the most prevalent neoplasms worldwide, ranking as the second leading cause of cancer-related death due to its high invasive and metastatic potential. SIRT1 (silent information regulator 1), a member of mammalian sirtuin family protein (SIRT1–SIRT7), functions as a conserved nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase to implicate in the modulation of transcriptional silencing and cell survival. Recently, except for the regulatory role of SIRT1 in various biological processes, the carcinogenesis effect of SIRT1 was revealed in HCC. Importantly, SIRT1 was confirmed to be involved in tumorigenesis, metastasis, prognosis, and chemical resistant of HCC, as a result of its deacetylation of oncogenic or tumor suppressor factors. The focus of this review was to delineate the carcinogenesis effects of SIRT1 on HCC and present an overview of SIRT1 functions in normal liver followed by SIRT1 roles in HCC, with focus on the underlying molecular mechanism to promote SIRT1 as a new therapeutic target for HCC.
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