Modification of Epigenetic Histone Acetylation in Hepatocellular Carcinoma

Liu, Kwei Yan; Wang, Li Ting; Hsu, Shih-Hsien

doi:10.3390/cancers10010008

Cited by 44 publications

(24 citation statements)

References 81 publications

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“…On the other hand, the inhibition of HDAC activity keeps a continuous expression of a target gene. In this context, the control of HDAC activity by HDAC inhibitors has been targeted for the development of anticancer strategies as well as therapies for human diseases derived from cardiovascular, metabolic, and neurodegenerative disorders [3][4][5][6][7][8] .…”

Section: Introductionmentioning

confidence: 99%

A short guide to histone deacetylases including recent progress on class II enzymes

2020

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The interaction between histones and DNA is important for eukaryotic gene expression. A loose interaction caused, for example, by the neutralization of a positive charge on the histone surface by acetylation, induces a less compact chromatin structure, resulting in feasible accessibility of RNA polymerase and increased gene expression. In contrast, the formation of a tight chromatin structure due to the deacetylation of histone lysine residues on the surface by histone deacetylases enforces the interaction between the histones and DNA, which minimizes the chance of RNA polymerases contacting DNA, resulting in decreased gene expression. Therefore, the balance of the acetylation of histones mediated by histone acetylases (HATs) and histone deacetylases (HDACs) is an issue of transcription that has long been studied in relation to posttranslational modification. In this review, current knowledge of HDACs is briefly described with an emphasis on recent progress in research on HDACs, especially on class IIa HDACs.

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Section: Introductionmentioning

confidence: 99%

A short guide to histone deacetylases including recent progress on class II enzymes

2020

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“…The majority of HCC patients are diagnosed in advanced stages of the disease, and the poor survival in patients with HCC can be largely attributed to rapid intrahepatic recurrence due to cancer metastases (24). HDAC inhibitors, including trichostatin A and vorinostat, induce cell death but simultaneously augment cell migration and metastasis to ruin therapeutic efficacy via activating protein kinase C signaling (25).…”

Section: Discussionmentioning

confidence: 99%

BAY 87‑2243 sensitizes hepatocellular carcinoma Hep3B cells to histone deacetylase inhibitors treatment via GSK‑3β activation

Rao

Zhang

et al. 2019

Exp Ther Med

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Hepatocellular carcinoma (HCC) is associated with some of the highest cancer-associated mortality rates. Histone deacetylase (HDAC) inhibitors anti-HCC activities have been shown to promote Snail-induced metastasis. In the present study, it was shown that BAY 87-2243, a hypoxia-inducible transcription factor-1α inhibitor, could enhance the anti-HCC effects of HDAC inhibitors, including trichostatin A and vorinostat. In addition, BAY 87-2243 plus HDAC inhibitors exhibited synergistic cytotoxicity and induced significant cell death in Hep3B cells. Additionally, BAY 87-2243 combined with HDAC inhibitors-treated Hep3B cells formed fewer and smaller colonies as compared with either the control or single agent-treated cells. Furthermore, glycogen synthase kinase-3β might be involved in the enhanced cell death induced by BAY 87-2243 plus HDAC inhibitors. The present data also indicated that BAY 87-2243 combined with HDAC inhibitors could suppress the migration of Hep3B cells, and BAY 87-2243 could reverse the HDAC inhibitor-induced Snail activation in Hep3B cells. In conclusion, BAY 87-2243 combined with HDAC inhibitors might be an attractive chemotherapy strategy for HCC therapy.

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“…The current investigation indicated that deregulation of HATs and histone HDACs is engaged in the progression of a range of cancers, making them spur the considerable interest of the research community [22,85]. Thus, HDACis become appealed target in attempts to attenuate many human cancers including colorectal cancer.…”

Section: Histone Deacetylase Inhibitors and The Treatment Of Colorectmentioning

confidence: 94%

Histone Modifications and their Role in Colorectal Cancer (Review)

Qin

Wen

Liang

et al. 2019

Pathol. Oncol. Res.

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The development of colorectal cancer is a complex and multistep process mediated by a variety of factors including the dysregulation of genetic and epigenetic under the influence of microenvironment. It is evident that epigenetics that affects gene activity and expression has been recognized as a critical role in the carcinogenesis. Aside from DNA methylation, miRNA level, and genomic imprinting, histone modification is increasingly recognized as an essential mechanism underlying the occurrence and development of colorectal cancer. Aberrant regulation of histone modification like acetylation, methylation and phosphorylation levels on specific residues is implicated in a wide spectrum of cancers, including colorectal cancer. In addition, as this process is reversible and accompanied by a plethora of deregulated enzymes, inhibiting those histone-modifying enzymes activity and regulating its level has been thought of as a potential path for tumor therapy. This review provides insight into the basic information of histone modification and its application in the colorectal cancer treatment, thereby offering new potential targets for treatment of colorectal cancer.

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Modification of Epigenetic Histone Acetylation in Hepatocellular Carcinoma

Cited by 44 publications

References 81 publications

A short guide to histone deacetylases including recent progress on class II enzymes

A short guide to histone deacetylases including recent progress on class II enzymes

BAY 87‑2243 sensitizes hepatocellular carcinoma Hep3B cells to histone deacetylase inhibitors treatment via GSK‑3β activation

Histone Modifications and their Role in Colorectal Cancer (Review)

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