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Article: Epigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas

TitleEpigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas
Authors
KeywordsEndometrial carcinoma
Metallothionein 1E gene
Promoter hypermethylation
Issue Date2009
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
Citation
Tumor Biology, 2009, v. 30 n. 2, p. 93-99 How to Cite?
AbstractAberrant expression of metallothioneins (MTs) has been observed in several human tumors. In our microarray analysis, MT-1E was found to have much lower expression in endometrial cancer cells as compared with other types of cancer cells generated from the cervix, ovary or prostate. The result was confirmed by quantitative RT-PCR analysis of the MT-1E levels in individual cancer cells. Treatment of endometrial cancer cells with 5-azacytidine could reactivate MT-1E expression. We further analyzed the DNA methylation status of the promoter region of MT-1E using methylation-sensitive restriction enzymes HhaI and HpaII, followed by PCR. Promoter hypermethylation was detected in 42.4% (53/125) of the endometrial carcinoma samples, whilst none of the 38 normal tissues or hyperplasia samples were methylated. The mRNA levels of MT-1E were significantly lower in the methylation-positive than in the methylation-negative samples. Endometrial carcinoma samples with low MT-1E expression coincidently had low levels of estrogen receptor-α expression and vice versa. This phenomenon was not observed in the expression pattern between estrogen receptor-β and MT-1E. There was no significant correlation between MT-1E methylation and any clinical parameters. In conclusion, a high frequency of cancer-specific hypermethylation of MT-1E was found in endometrial carcinomas. Its functional consequence in the development of endometrial cancer warrants further investigation. Copyright © 2009 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/60340
ISSN
2014 Impact Factor: 3.611
2014 SCImago Journal Rankings: 0.882
ISI Accession Number ID
Funding AgencyGrant Number
Wong Check She Charitable Foundation
Hospital Authority, Hong Kong
Funding Information:

This study was supported by the Wong Check She Charitable Foundation and in part by the Training and Research Assistance Scheme of the Hospital Authority, Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorTse, KYen_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorChan, DWen_HK
dc.contributor.authorChiu, PMen_HK
dc.contributor.authorTam, KFen_HK
dc.contributor.authorChan, KKLen_HK
dc.contributor.authorLiao, XYen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorNgan, HYSen_HK
dc.date.accessioned2010-05-31T04:08:40Z-
dc.date.available2010-05-31T04:08:40Z-
dc.date.issued2009en_HK
dc.identifier.citationTumor Biology, 2009, v. 30 n. 2, p. 93-99en_HK
dc.identifier.issn1010-4283en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60340-
dc.description.abstractAberrant expression of metallothioneins (MTs) has been observed in several human tumors. In our microarray analysis, MT-1E was found to have much lower expression in endometrial cancer cells as compared with other types of cancer cells generated from the cervix, ovary or prostate. The result was confirmed by quantitative RT-PCR analysis of the MT-1E levels in individual cancer cells. Treatment of endometrial cancer cells with 5-azacytidine could reactivate MT-1E expression. We further analyzed the DNA methylation status of the promoter region of MT-1E using methylation-sensitive restriction enzymes HhaI and HpaII, followed by PCR. Promoter hypermethylation was detected in 42.4% (53/125) of the endometrial carcinoma samples, whilst none of the 38 normal tissues or hyperplasia samples were methylated. The mRNA levels of MT-1E were significantly lower in the methylation-positive than in the methylation-negative samples. Endometrial carcinoma samples with low MT-1E expression coincidently had low levels of estrogen receptor-α expression and vice versa. This phenomenon was not observed in the expression pattern between estrogen receptor-β and MT-1E. There was no significant correlation between MT-1E methylation and any clinical parameters. In conclusion, a high frequency of cancer-specific hypermethylation of MT-1E was found in endometrial carcinomas. Its functional consequence in the development of endometrial cancer warrants further investigation. Copyright © 2009 S. Karger AG, Basel.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBIen_HK
dc.relation.ispartofTumor Biologyen_HK
dc.subjectEndometrial carcinomaen_HK
dc.subjectMetallothionein 1E geneen_HK
dc.subjectPromoter hypermethylationen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEndometrial Neoplasms - genetics - metabolismen_HK
dc.subject.meshEpigenesis, Geneticen_HK
dc.subject.meshEstrogen Receptor alpha - genetics - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMetallothionein - genetics - metabolismen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.titleEpigenetic alteration of the metallothionein 1e gene in human endometrial carcinomasen_HK
dc.typeArticleen_HK
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.emailChan, DW: dwchan@hku.hken_HK
dc.identifier.emailChan, KKL: kklchan@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.identifier.authorityChan, DW=rp00543en_HK
dc.identifier.authorityChan, KKL=rp00499en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000218032en_HK
dc.identifier.pmid19420986en_HK
dc.identifier.scopuseid_2-s2.0-65449153636en_HK
dc.identifier.hkuros157706en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65449153636&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue2en_HK
dc.identifier.spage93en_HK
dc.identifier.epage99en_HK
dc.identifier.isiWOS:000266098000006-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridTse, KY=8876026900en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridChan, DW=26533900600en_HK
dc.identifier.scopusauthoridChiu, PM=7103182596en_HK
dc.identifier.scopusauthoridTam, KF=7201692816en_HK
dc.identifier.scopusauthoridChan, KKL=8655666700en_HK
dc.identifier.scopusauthoridLiao, XY=7202134156en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK

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