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Conference Paper: Down-regulation of ID4 by promoter hypermethylation in gastric adenocarcinoma

TitleDown-regulation of ID4 by promoter hypermethylation in gastric adenocarcinoma
Authors
Issue Date2003
PublisherIOS PRess.
Citation
The 2003 International Conference on Applied Genomics (ICAG 2003) : 9th European Society for Analytical Cellular Pathology Meeting (ESACP) and 16th International Society for Diagnostic Quantitative Pathology Meeting(ISDQP), Amsterdam, The Netherlands, 1-4 October 2003. In Analytical Cellular Pathology, v. 25, p. 250, abstract no. A.04 How to Cite?
AbstractPromoter hypermethylation has become apparent as a common mechanism of gene silencing in cancer. Based on our published microarray expression data, we noticed a prominent down-regulation of ID4 in gastric adenocarcinoma. The dense 5 CpG island covering the previously mapped upstream promoter of ID4 has prompted us to relate its down-regulation to promoter hypermethylation. ID proteins are distinct members in the helix-loop-helix family of transcriptional regulators, which modulate various key developmental processes. Emerging data have suggested the involvement of ID genes in tumorigenesis. In this study using bisulphite genomic sequencing, we have found hypermethylation of ID4 promoter in most gastric cancer cell lines and 30% of primary tumors. This correlated with decreased level of ID4 expression. Restoration of ID4 expression in various gastric cancer cell lines was achieved by treatment with the DNA methyltransferase inhibitor 5-aza-2 -deoxycytidine, which at times required the synergistic action of the histone deacetylase inhibitor trichostatin A, but not with trichostatin A alone. Re-expression was accompanied by the corresponding ID4 promoter demethylation. Furthermore, we have found significant association of ID4 promoter methylation with hMLH1 promoter methylation (p = 0.008) and microsatellite instability (p = 0.006). Overall, our results have shown that transcriptional silencing of ID4 is related to the aberrant methylation of its promoter in gastric cancer. The significant association of ID4 and hMLH1 promoter hypermethylation suggested that ID4 may also be among the genes being targeted in the CpG island methylator phenotype tumorigenic pathway
DescriptionICAG 2003: Poster sessions
Persistent Identifierhttp://hdl.handle.net/10722/104865
ISSN
2005 Impact Factor: 1.3
2006 SCImago Journal Rankings: 0.770

 

DC FieldValueLanguage
dc.contributor.authorChan, ASW-
dc.contributor.authorTsui, WY-
dc.contributor.authorChen, X-
dc.contributor.authorChu, KM-
dc.contributor.authorChan, CTL-
dc.contributor.authorChan, ASY-
dc.contributor.authorLi, R-
dc.contributor.authorSo, S-
dc.contributor.authorYuen, ST-
dc.contributor.authorLeung, SY-
dc.date.accessioned2010-09-25T22:10:33Z-
dc.date.available2010-09-25T22:10:33Z-
dc.date.issued2003-
dc.identifier.citationThe 2003 International Conference on Applied Genomics (ICAG 2003) : 9th European Society for Analytical Cellular Pathology Meeting (ESACP) and 16th International Society for Diagnostic Quantitative Pathology Meeting(ISDQP), Amsterdam, The Netherlands, 1-4 October 2003. In Analytical Cellular Pathology, v. 25, p. 250, abstract no. A.04-
dc.identifier.issn0921-8912-
dc.identifier.urihttp://hdl.handle.net/10722/104865-
dc.descriptionICAG 2003: Poster sessions-
dc.description.abstractPromoter hypermethylation has become apparent as a common mechanism of gene silencing in cancer. Based on our published microarray expression data, we noticed a prominent down-regulation of ID4 in gastric adenocarcinoma. The dense 5 CpG island covering the previously mapped upstream promoter of ID4 has prompted us to relate its down-regulation to promoter hypermethylation. ID proteins are distinct members in the helix-loop-helix family of transcriptional regulators, which modulate various key developmental processes. Emerging data have suggested the involvement of ID genes in tumorigenesis. In this study using bisulphite genomic sequencing, we have found hypermethylation of ID4 promoter in most gastric cancer cell lines and 30% of primary tumors. This correlated with decreased level of ID4 expression. Restoration of ID4 expression in various gastric cancer cell lines was achieved by treatment with the DNA methyltransferase inhibitor 5-aza-2 -deoxycytidine, which at times required the synergistic action of the histone deacetylase inhibitor trichostatin A, but not with trichostatin A alone. Re-expression was accompanied by the corresponding ID4 promoter demethylation. Furthermore, we have found significant association of ID4 promoter methylation with hMLH1 promoter methylation (p = 0.008) and microsatellite instability (p = 0.006). Overall, our results have shown that transcriptional silencing of ID4 is related to the aberrant methylation of its promoter in gastric cancer. The significant association of ID4 and hMLH1 promoter hypermethylation suggested that ID4 may also be among the genes being targeted in the CpG island methylator phenotype tumorigenic pathway-
dc.languageeng-
dc.publisherIOS PRess. -
dc.relation.ispartofAnalytical Cellular Pathology-
dc.titleDown-regulation of ID4 by promoter hypermethylation in gastric adenocarcinoma-
dc.typeConference_Paper-
dc.identifier.emailChan, ASW: chansw3@hku.hk-
dc.identifier.emailTsui, WY: wtsui112@hkucc.hku.hk-
dc.identifier.emailChu, KM: chukm@hkucc.hku.hk-
dc.identifier.emailChan, CTL: tlchan@hku.hk-
dc.identifier.emailChan, ASY: asychan@hku.hk-
dc.identifier.emailYuen, ST: styuen@hku.hk-
dc.identifier.emailLeung, SY: suetyi@hkucc.hku.hk-
dc.identifier.authorityChu, KM=rp00435-
dc.identifier.authorityChan, CTL=rp00418-
dc.identifier.authorityLeung, SY=rp00359-
dc.identifier.hkuros86167-
dc.identifier.volume25-
dc.identifier.spage250, abstract no. A.04-
dc.identifier.epage250, abstract no. A.04-
dc.publisher.placeThe Netherlands-

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