ArticleMolecular cancer2002
Reactivation of a silenced H19 gene in human rhabdomyosarcoma by demethylation of DNA but not by histone hyperacetylation.
Article in Molecular cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 254 citations in OpenAlex.
- Clinical Significance and Therapeutic Potential of Long Non-Coding RNA H19 in Soft Tissue Sarcoma.Cancer medicine · 2026Article
- Epigenetic paradigm of DNA methylation for understanding the pathophysiology, diagnostics, and therapeutics in sarcomas.Epigenomics · 2025Review
- Hypomethylation at H19DMR in penile squamous cell carcinoma is not related to HPV infection.Epigenetics · 2024Article
- A review of the therapeutic potential of histone deacetylase inhibitors in rhabdomyosarcoma.Frontiers in oncology · 2023Review
- Long Non-Coding RNAs in Pancreatic Cancer: Biologic Functions, Mechanisms, and Clinical Significance.Cancers · 2022Review
- Long noncoding RNA H19 - a new player in the pathogenesis of liver diseases.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Small molecules capable of activating DNA methylation-repressed genes targeted by the p38 mitogen-activated protein kinase pathway.The Journal of biological chemistry · 2018Article
- Genomic Imprinting and the Regulation of Postnatal Neurogenesis.Brain plasticity (Amsterdam, Netherlands) · 2017Review
- The long noncoding RNA H19 promotes cell proliferation via E2F-1 in pancreatic ductal adenocarcinoma.Cancer biology & therapy · 2016Article
- Review
- The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration.Genes & development · 2014Article
- Enhanced angiogenic and cardiomyocyte differentiation capacity of epigenetically reprogrammed mouse and human endothelial progenitor cells augments their efficacy for ischemic myocardial repair.Circulation research · 2012Article
- Chromatin structure predicts epigenetic therapy responsiveness in sarcoma.Molecular cancer therapeutics · 2011Article
- Regulation of demethylation and re-expression of RASSF1A gene in gastric cancer cell lines by combined treatment of 5-Aza-CdR and NaB.World journal of gastroenterology · 2008Article
- Allele-specific histone modifications regulate expression of the Dlk1-Gtl2 imprinted domain.Genomics · 2007Article
- H19 expression in hepatic metastases from a range of human carcinomas.Journal of clinical pathology · 2005Article
- Mutations in the IGF-II pathway that confer resistance to lytic reovirus infection.BMC cell biology · 2004Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe active copy of the imprinted gene H19 is turned off by inappropriate methylation in several pediatric tumors including Wilms' Tumour and embryonal rhabdomyosarcoma. H19 controls in cis the linked Insulin-like Growth Factor 2 (IGF2) gene, encoding an important growth factor. Recent work has suggested that methylation of a gene may lead to deacetylation of its associated histones and that silenced genes can be reactivated by increasing histone acetylation levels.
resultsTreatment of a rhabdomyosarcoma cell line which has a silent, methylated H19 gene with histone deacetylase (HDAC) inhibitors under conditions which gave maximal hyperacetylation of histone 4, both globally and at the H19 gene itself could not reactivate H19 or affect the active Insulin-like Growth Factor 2 (IGF2) gene, but caused clear up-regulation of the Tissue-type Plasminogen Activator (TPA) gene, a non-imprinted gene known to respond to changes in histone acetylation. In contrast, mild treatment of the cells with the methylation inhibitor 5-AzaC-2'-deoxycytidine (AzaC) on its own was able to reactivate H19. Combining AzaC treatment with HDAC inhibitors gave a reduced rather than enhanced reactivation. These findings were confirmed in mouse primary liver and kidney explants which maintain normal imprinting, where we also found that the silent Igf2 gene could not be reactivated by HDAC inhibitors.
conclusionThese results suggest that DNA methylation rather than histone acetylation is the primary determinant of silencing of H19 in rhabdomyosarcoma.
Indexed as
Identifiers
12234381PMC119368W2122455451What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.