Histone deacetylase 3 participates in self-renewal of liver cancer stem cells through histone modification

Liu, Chungang; Liu, Limei; Shan, Juanjuan; Shen, Junjie; Xu, Yan; Zhang, Qianzhen; Yang, Zhi; Wu, Lin; Xia, Feng; Bie, Ping; Cui, You‐Hong; Zhang, Xia; Bian, Xiu‐Wu; Qian, Cheng

doi:10.1016/j.canlet.2013.07.022

Cited by 74 publications

(60 citation statements)

References 37 publications

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“…HDAC3 was selectively expressed in the liver for self-renewal of cancer stem cells and plays a critical role in regulating liver cancer stem cells. 54 In HCC cells, up-regulation of HDAC1-3 reduces expression of miR-449. MiR-449 can promote apoptosis and reduce proliferation of liver cells through targeting c-MET mRNA that encodes the receptor tyrosine kinase for the hepatocyte growth factor.…”

Section: Hdacs and Hepatocellular Carcinomamentioning

confidence: 99%

Histone Deacetylases and Mechanisms of Regulation of Gene Expression

2015

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In recent years, it has become widely recognized that histone modification plays a pivotal role in controlling gene expression, and is involved in a wide spectrum of disease regulation. Histone acetylation is a major modification that affects gene transcription and is controlled by histone acetyltransferases (HATs) and histone deacetylases (HDAC). HATs acetylate lysines of histone proteins, resulting in relaxation of chromatin structure, and they also facilitate gene activation. Conversely, HDACs remove acetyl groups from hyperacetylated histones and suppress general gene transcription. In addition to histones, numerous non-histone proteins can be acetylated and deacetylated, and they are also involved in a wide range of disease regulation. To date, there are 18 HDACs in mammals classified into four classes based on homology to yeast HDACs. Accumulating evidence has revealed that HDACs play crucial roles in a variety of biological processes including inflammation, cell proliferation, apoptosis, and carcinogenesis. In this review, we summarize the current state of knowledge of HDACs in carcinogenesis and describe the involvement of HDACs in cancer-associated molecular processes. It is hoped than our understanding of the role of HDACs in cancer will lead to the design of more potent and specific drugs targeting selective HDAC proteins for the treatment of the disease.

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Section: Hdacs and Hepatocellular Carcinomamentioning

confidence: 99%

Histone Deacetylases and Mechanisms of Regulation of Gene Expression

2015

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“…Increased expressions of HDAC3 have been found closely associated with many malignancies (5). In several studies analyzing patient cancer samples, overexpression of HDAC3 was found in hepatocellular (17), lung (18) and prostate carcinomas (19) and in most of the cases HDAC3 upregulation associates with poor prognosis. Also it was proposed to serve as a candidate biomarker (20).…”

Section: Discussionmentioning

confidence: 99%

Histone deacetylase 3 promotes pancreatic cancer cell proliferation, invasion and increases drug-resistance through histone modification of P27, P53 and Bax

Jiao

Yuan

et al. 2014

International Journal of Oncology

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Abstract. Pancreatic cancer is one of the most aggressive solid malignancies with a dismal survival rate. Recent studies have shown that high expression levels of histone deacetylase 3 (HDAC3) correlate with malignant phenotype. However, the expression patterns and biological role of HDAC3 in pancreatic cancer remain unclear. In this study, our data showed that a higher level of HDAC3 protein expression was found in pancreatic cancer as compared to paired paracancerous tissues. Consistently, higher expression level of HDAC3 was found in all of the eight pancreatic cancer cell lines relative to human pancreatic ductal epithelial cells (HPDE). In addition, further function analysis revealed that HDAC3 can function as oncogenic protein, which could promote pancreatic cancer cell proliferation, migration and invasion, and may increase drug resistance. Moreover, the functional involvement of HDAC3 was partially correlated with post-induction repression of P53, P27 and Bax gene transcription, acting via H3K9 deacetylation. Taken together, our data suggest that HDAC3 participates in the pathogenesis and progression of pancreatic cancer through histone modification, which might be a pivotal epigenetic target against this devastating disease.

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“…112 Overexpression of HDAC3 is also correlated with advanced tumour stage and early recurrence after surgery. 113 HDAC inhibitors (HDACi) have had favourable preclinical results, and induce apoptosis in tumour cells 114 Pabinostat, a hydroxamic acid, pan-HDACi, when combined with sorafenib, demonstrated efficacy in HCC xenograft models. 115 In humans, efficacy of HDACi has been demonstrated in advanced cutaneous and peripheral T-cell lymphoma.…”

Section: Hdac Inhibitorsmentioning

confidence: 99%

Epigenetics in liver disease: from biology to therapeutics

Hardy

Mann

2016

Gut

129

140

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Knowledge of the fundamental epigenetic mechanisms governing gene expression and cellular phenotype are sufficiently advanced that novel insights into the epigenetic control of chronic liver disease are now emerging. Hepatologists are in the process of shedding light on the roles played by DNA methylation, histone/chromatin modifications and non-coding RNAs in specific liver pathologies. Alongside these discoveries are advances in the technologies for the detection and quantification of epigenetic biomarkers, either directly from patient tissue or from body fluids. The premise for this review is to survey the recent advances in the field of liver epigenetics and to explore their potential for translation by industry and clinical hepatologists for the design of novel therapeutics and diagnostic/prognostic biomarkers. In particular, we present findings in the context of hepatocellular carcinoma, fibrosis and non-alcoholic fatty liver disease, where there is urgent unmet need for new clinical interventions and biomarkers.

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Histone deacetylase 3 participates in self-renewal of liver cancer stem cells through histone modification

Cited by 74 publications

References 37 publications

Histone Deacetylases and Mechanisms of Regulation of Gene Expression

Histone Deacetylases and Mechanisms of Regulation of Gene Expression

Histone deacetylase 3 promotes pancreatic cancer cell proliferation, invasion and increases drug-resistance through histone modification of P27, P53 and Bax

Epigenetics in liver disease: from biology to therapeutics

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