Modification of epigenetic histone acetylation in hepatocellular carcinoma

Kwei Yan Liu, Li Ting Wang, Shih Hsien Hsu*

*此作品的通信作者

研究成果: 雜誌貢獻回顧評介論文同行評審

27 引文 斯高帕斯(Scopus)

摘要

Cells respond to various environmental factors such as nutrients, food intake, and drugs or toxins by undergoing dynamic epigenetic changes. An imbalance in dynamic epigenetic changes is one of the major causes of disease, oncogenic activities, and immunosuppressive effects. The aryl hydrocarbon receptor (AHR) is a unique cellular chemical sensor present in most organs, and its dysregulation has been demonstrated in multiple stages of tumor progression in humans and experimental models; however, the effects of the pathogenic mechanisms of AHR on epigenetic regulation remain unclear. Apart from proto-oncogene activation, epigenetic repressions of tumor suppressor genes are involved in tumor initiation, procession, and metastasis. Reverse epigenetic repression of the tumor suppressor genes by epigenetic enzyme activity inhibition and epigenetic enzyme level manipulation is a potential path for tumor therapy. Current evidence and our recent work on deacetylation of histones on tumor-suppressive genes suggest that histone deacetylase (HDAC) is involved in tumor formation and progression, and treating hepatocellular carcinoma with HDAC inhibitors can, at least partially, repress tumor proliferation and transformation by recusing the expression of tumor-suppressive genes such as TP53 and RB1.

原文英語
文章編號8
期刊Cancers
10
發行號1
DOIs
出版狀態已發佈 - 2018 一月
對外發佈

ASJC Scopus subject areas

  • 腫瘤科
  • 癌症研究

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