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Article: Transcriptional repressive H3K9 and H3K27 methylations contribute to DNMT1-mediated DNA methylation recovery

TitleTranscriptional repressive H3K9 and H3K27 methylations contribute to DNMT1-mediated DNA methylation recovery
Authors
KeywordsCytokeratin 19
Histone h3
Demethylation
DNA methylation
Epigenetics
Issue Date2011
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2011, v. 6 n. 2 How to Cite?
AbstractDNA methylation and histone modifications are two major epigenetic events regulating gene expression and chromatin structure, and their alterations are linked to human carcinogenesis. DNA methylation plays an important role in tumor suppressor gene inactivation, and can be revised by DNA methylation inhibitors. The reversible nature of DNA methylation forms the basis of epigenetic cancer therapy. However, it has been reported that DNA re-methylation and gene re-silencing could occur after removal of demethylation treatment and this may significantly hamper the therapeutic value of DNA methylation inhibitors. In this study we have provided detailed evidence demonstrating that mammalian cells possess a bona fide DNA methylation recovery system. We have also shown that DNA methylation recovery was mediated by the major human DNA methyltransferase, DNMT1. In addition, we found that H3K9-tri-methylation and H3K27-tri-methylation were closely associated with this DNA methylation recovery. These persistent transcriptional repressive histone modifications may have a crucial role in regulating DNMT1-mediated DNA methylation recovery. Our findings may have important implications towards a better understanding of epigenetic regulation and future development of epigenetic therapeutic intervention. © 2011 Wong et al.
Persistent Identifierhttp://hdl.handle.net/10722/137626
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilHKU 1/06C
HKU 7/CRG/09
Michael and Betty Kadoorie Cancer Genetics Research Program
Funding Information:

The study was supported by Hong Kong Research Grants Council Collaborative Research Fund (HKU 1/06C and HKU 7/CRG/09) and Michael and Betty Kadoorie Cancer Genetics Research Program 2004. I.O.L. Ng is Loke Yew Professor in Pathology. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWong, CMen_HK
dc.contributor.authorWong, CCLen_HK
dc.contributor.authorNg, YLen_HK
dc.contributor.authorAu, SLKen_HK
dc.contributor.authorKo, FCFen_HK
dc.contributor.authorNg, IOLen_HK
dc.date.accessioned2011-08-26T14:29:38Z-
dc.date.available2011-08-26T14:29:38Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 2en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137626-
dc.description.abstractDNA methylation and histone modifications are two major epigenetic events regulating gene expression and chromatin structure, and their alterations are linked to human carcinogenesis. DNA methylation plays an important role in tumor suppressor gene inactivation, and can be revised by DNA methylation inhibitors. The reversible nature of DNA methylation forms the basis of epigenetic cancer therapy. However, it has been reported that DNA re-methylation and gene re-silencing could occur after removal of demethylation treatment and this may significantly hamper the therapeutic value of DNA methylation inhibitors. In this study we have provided detailed evidence demonstrating that mammalian cells possess a bona fide DNA methylation recovery system. We have also shown that DNA methylation recovery was mediated by the major human DNA methyltransferase, DNMT1. In addition, we found that H3K9-tri-methylation and H3K27-tri-methylation were closely associated with this DNA methylation recovery. These persistent transcriptional repressive histone modifications may have a crucial role in regulating DNMT1-mediated DNA methylation recovery. Our findings may have important implications towards a better understanding of epigenetic regulation and future development of epigenetic therapeutic intervention. © 2011 Wong et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCytokeratin 19-
dc.subjectHistone h3-
dc.subjectDemethylation-
dc.subjectDNA methylation-
dc.subjectEpigenetics-
dc.titleTranscriptional repressive H3K9 and H3K27 methylations contribute to DNMT1-mediated DNA methylation recoveryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=6&issue=2, abstract no. e6702&spage=1&epage=11&date=2011&atitle=Transcriptional+repressive+H3K9+and+H3K27+methylations+contribute+to+DNMT1-mediated+DNA+methylation+recoveryen_US
dc.identifier.emailWong, CM:jackwong@pathology.hku.hken_HK
dc.identifier.emailWong, CCL:carmencl@pathology.hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.authorityWong, CM=rp00231en_HK
dc.identifier.authorityWong, CCL=rp01602en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0016702en_HK
dc.identifier.pmid21347439-
dc.identifier.pmcidPMC3035659-
dc.identifier.scopuseid_2-s2.0-79951570106en_HK
dc.identifier.hkuros190837en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79951570106&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue2en_HK
dc.identifier.spage1en_US
dc.identifier.epage11en_US
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000287077600020-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectMolecular pathology of liver cancer - a multidisciplinary study-
dc.identifier.scopusauthoridWong, CM=16314668400en_HK
dc.identifier.scopusauthoridWong, CCL=24823630000en_HK
dc.identifier.scopusauthoridNg, YL=16313440600en_HK
dc.identifier.scopusauthoridAu, SLK=36460622800en_HK
dc.identifier.scopusauthoridKo, FCF=14630572500en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.citeulike9697731-

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