ArticleThe Journal of biological chemistry2010
H3K27 trimethylation is an early epigenetic event of p16INK4a silencing for regaining tumorigenesis in fusion reprogrammed hepatoma cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- Histone Methylation: A Pivotal Epigenetic Driver of the Malignant Transformation of MASLD-HCC.Journal of hepatocellular carcinoma · 2026Review
- A New CYP2E1 Inhibitor, 12-Imidazolyl-1-dodecanol, Represents a Potential Treatment for Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2021Article
- Epigenetic regulation of histone H3 in the process of hepatocellular tumorigenesis.Bioscience reports · 2019Review
- LncRNA-ANCR down-regulation suppresses invasion and migration of colorectal cancer cells by regulating EZH2 expression.Cancer biomarkers : section A of Disease markers · 2017Article
- Tumorigenic potential is restored during differentiation in fusion-reprogrammed cancer cells.Cell death & disease · 2016Article
- Altered primary chromatin structures and their implications in cancer development.Cellular oncology (Dordrecht, Netherlands) · 2016Review
- Hepatoepigenetic Alterations in Viral and Nonviral-Induced Hepatocellular Carcinoma.BioMed research international · 2016Review
- Role of epigenetic aberrations in the development and progression of human hepatocellular carcinoma.Cancer letters · 2014Review
- RNAi screening with shRNAs against histone methylation-related genes reveals determinants of sorafenib sensitivity in hepatocellular carcinoma cells.International journal of clinical and experimental pathology · 2014Article
- Article
- Clinical significance of cell cycle inhibitors in hepatocellular carcinoma.Medical molecular morphology · 2013Review
- Promoter and histone methylation and p16(INK4A) gene expression in colon cancer.Experimental and therapeutic medicine · 2012Article
- Environmental chemical exposures and human epigenetics.International journal of epidemiology · 2012Article
- From hepatitis to hepatocellular carcinoma: a proposed model for cross-talk between inflammation and epigenetic mechanisms.Genome medicine · 2012Article
- Nucleosomes correlate with in vivo progression pattern of de novo methylation of p16 CpG islands in human gastric carcinogenesis.PloS one · 2012Article
- Breast cancer cells induce stromal fibroblasts to secrete ADAMTS1 for cancer invasion through an epigenetic change.PloS one · 2012Article
- The association between non-Hodgkin lymphoma and methylation of p73.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011Article
- High expression of H3K27me3 in human hepatocellular carcinomas correlates closely with vascular invasion and predicts worse prognosis in patients.Molecular medicine (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Stable epigenetic silencing of p16(INK4a) is a common event in hepatocellular carcinoma (HCC) cells, which is associated with abnormal cell proliferation and liberation from cell cycle arrest. Understanding the early epigenetic events in silencing p16(INK4a) expression may illuminate a prognostic strategy to block HCC development. Toward this end, we created a reprogram cell model by the fusion mouse HCC cells with mouse embryonic stem cells, in which the ES-Hepa hybrids forfeited HCC cell characteristics along with reactivation of the silenced p16(INK4a). HCC characteristics, in terms of gene expression pattern and tumorigenic potential, was restored upon induced differentiation of these reprogrammed ES-Hepa hybrids. The histone methylation pattern relative to p16(INK4a) silencing during differentiation of the ES-Hepa hybrids was analyzed. H3K27 trimethylation at the p16(INK4a) promoter region, occurring in the early onset of p16(INK4a) silencing, was followed by H3K9 dimethylation at later stages. During the induced differentiation of the ES-Hepa hybrids, H3K4 di- and trimethylations were maintained at high levels during the silencing of p16(INK4a), strongly suggesting that H3K4 methylation events did not cause the silencing of p16(INK4a). Our results suggested that the enrichment of H3K27 trimethylation, independent of H3K9 dimethylation, trimethylation, and DNA methylation, was an early event in the silencing of p16(INK4a) during the tumor development. This unique chromatin pattern may be a heritable marker of epigenetic regulation for p16(INK4a) silencing during the developmental process of hepatocellular carcinogenesis.
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