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Conference Paper: 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
Issue Date2011
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 102th Annual Meeting of the American Association for Cancer Research (AACR), Orlando, Florida, USA, 2-6 April 2011. In Cancer Research, 2011, v. 71 n. 8 suppl., abstract no. 3020 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. Moreover, the DNA methylation recovery function of DNMT1 was cell division-independent and likely to be distinct from its conventional “maintenance” DNA methyltransferase function. 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.
DescriptionPoster Session 7, PO.CB06.02. Epigenetic Mechanisms and Methods, Abstract Number: 3020
Persistent Identifierhttp://hdl.handle.net/10722/137849
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, CM-
dc.contributor.authorWong, CCL-
dc.contributor.authorNg, YL-
dc.contributor.authorAu, LK-
dc.contributor.authorKo, FCF-
dc.contributor.authorNg, IOL-
dc.date.accessioned2011-08-26T14:35:09Z-
dc.date.available2011-08-26T14:35:09Z-
dc.date.issued2011-
dc.identifier.citationThe 102th Annual Meeting of the American Association for Cancer Research (AACR), Orlando, Florida, USA, 2-6 April 2011. In Cancer Research, 2011, v. 71 n. 8 suppl., abstract no. 3020-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/137849-
dc.descriptionPoster Session 7, PO.CB06.02. Epigenetic Mechanisms and Methods, Abstract Number: 3020-
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. Moreover, the DNA methylation recovery function of DNMT1 was cell division-independent and likely to be distinct from its conventional “maintenance” DNA methyltransferase function. 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.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleTranscriptional repressive H3K9 and H3K27 methylations contribute to DNMT1-mediated DNA methylation recovery-
dc.typeConference_Paper-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0197-016X&volume=&spage=&epage=&date=2011&atitle=Transcriptional+repressive+H3K9+and+H3K27+methylations+contribute+to+DNMT1-mediated+DNA+methylation+recovery-
dc.identifier.emailWong, CM: jackwong@pathology.hku.hk-
dc.identifier.emailWong, CCL: carmencl@pathology.hku.hk-
dc.identifier.emailKo, FCF: bokcf@hku.hk-
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hk-
dc.identifier.authorityWong, CM=rp00231-
dc.identifier.authorityWong, CCL=rp01602-
dc.identifier.authorityNg, IOL=rp00335-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/1538-7445.AM2011-3020-
dc.identifier.hkuros191366-
dc.identifier.volume71-
dc.identifier.issue8 suppl., abstract no. 3020-
dc.publisher.placeUnited States-

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