ArticleJournal of cancer research and clinical oncology2008
Overexpression of myocyte enhancer factor 2 and histone hyperacetylation in hepatocellular carcinoma.
Article in Journal of cancer research and clinical oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 87 citations in OpenAlex.
- Trial
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- Construction of a prognostic model for gastric cancer based on immune infiltration and microenvironment, and exploration of MEF2C gene function.BMC medical genomics · 2025Article
- Acetylation of Histone H3 in Cancer Progression and Prognosis.International journal of molecular sciences · 2024Review
- Prostate Cancer: Genetics, Epigenetics and the Need for Immunological Biomarkers.International journal of molecular sciences · 2023Review
- Cancer and Alzheimer's Inverse Correlation: an Immunogenetic Analysis.Molecular neurobiology · 2023Review
- Geldanamycin treatment does not result in anti-cancer activity in a preclinical model of orthotopic mesothelioma.PloS one · 2023Article
- Comprehensive bioinformatics analysis forTranslational cancer research · 2022Article
- Transcriptome Analysis Reveals the Anti-cancerous Mechanism of Licochalcone A on Human Hepatoma Cell HepG2.Frontiers in nutrition · 2021Article
- The Role of Histone Acetylation-/Methylation-Mediated Apoptotic Gene Regulation in Hepatocellular Carcinoma.International journal of molecular sciences · 2020Review
- Myocyte-specific enhancer factor 2D promotes tumorigenesis and progression in tongue squamous cell carcinoma.International journal of clinical and experimental pathology · 2020Article
- Enzymatic and nonenzymatic protein acetylations control glycolysis process in liver diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Review
- Photoelectrochemical determination of the activity of histone acetyltransferase and inhibitor screening by using MoSMikrochimica acta · 2019Article
- p53 at the Crossroads between Different Types of HDAC Inhibitor-Mediated Cancer Cell Death.International journal of molecular sciences · 2019Review
- Anticancer effect of histone deacetylase inhibitor scriptaid as a single agent for hepatocellular carcinoma.Bioscience reports · 2018Article
- Acetylation and deacetylation in cancer stem-like cells.Oncotarget · 2017Review
- Article
- The co-existence of transcriptional activator and transcriptional repressor MEF2 complexes influences tumor aggressiveness.PLoS genetics · 2017Article
- Myocyte enhancer factor 2D provides a cross-talk between chronic inflammation and lung cancer.Journal of translational medicine · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIt has been indicated that activated hepatic stellate cells (HSCs) play key roles on the pathogenesis of hepatocellular carcinoma (HCC). The purpose of the study was to investigate the potential mechanism in it.
methodsActivation of HSCs, the expression of myocyte enhancer factor 2 (MEF2), class II histone deacetylases (II HDACs) and histone acetylation were analyzed in specimens of primary HCCs, cirrhotic and normal livers. Activated HSCs were identified using anti-a-smooth muscle actin (a-SMA) by Immunohistochemistry (IHC). The levels of expression of MEF2A, MEF2C and II HDACs mRNA and protein were measured by real time quantitative PCR and western blot (WB). Histone acetylation was assessed using anti-acetyl-histone H3, -H4 by WB and IHC. A P value < 0.05 was considered statistically significant.
resultsA-SMA positive activated HSCs were more prominent in HCCs and cirrhotic livers than in normal livers, accompanied by marked expression of MEF2A and MEF2C. The expression of MEF2A, MEF2C and II HDACs, both mRNA and protein, were much more enhanced in HCCs than those in cirrhotic and normal livers (P < 0.05). Histone H3 and H4 were hyperacetylated in HCCs compared with those in cirrhotic and normal livers (P < 0.05). The correlation coefficients between the expression of MEF2 and II HDACs, acetyl-histones were all beyond 0.5.
conclusionsThese data showed a potential molecular mechanism that activated HSCs participate in the pathogenesis of HCCs by overexpression of MEF2 and its consequent impact on histone hyperacetylation. Further investigations aimed at interfering MEF2 expression are needed.
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