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Article: Epigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas
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TitleEpigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas
 
AuthorsTse, KY1
Liu, VWS1
Chan, DW1
Chiu, PM1
Tam, KF1
Chan, KKL1
Liao, XY1
Cheung, ANY1
Ngan, HYS1
 
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
 
CitationTumor Biology, 2009, v. 30 n. 2, p. 93-99 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000218032
 
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.
 
ISSN1010-4283
2012 Impact Factor: 2.518
2012 SCImago Journal Rankings: 0.813
 
DOIhttp://dx.doi.org/10.1159/000218032
 
ISI Accession Number IDWOS:000266098000006
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorTse, KY
 
dc.contributor.authorLiu, VWS
 
dc.contributor.authorChan, DW
 
dc.contributor.authorChiu, PM
 
dc.contributor.authorTam, KF
 
dc.contributor.authorChan, KKL
 
dc.contributor.authorLiao, XY
 
dc.contributor.authorCheung, ANY
 
dc.contributor.authorNgan, HYS
 
dc.date.accessioned2010-05-31T04:08:40Z
 
dc.date.available2010-05-31T04:08:40Z
 
dc.date.issued2009
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationTumor Biology, 2009, v. 30 n. 2, p. 93-99 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000218032
 
dc.identifier.doihttp://dx.doi.org/10.1159/000218032
 
dc.identifier.epage99
 
dc.identifier.hkuros157706
 
dc.identifier.isiWOS:000266098000006
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.

 
dc.identifier.issn1010-4283
2012 Impact Factor: 2.518
2012 SCImago Journal Rankings: 0.813
 
dc.identifier.issue2
 
dc.identifier.pmid19420986
 
dc.identifier.scopuseid_2-s2.0-65449153636
 
dc.identifier.spage93
 
dc.identifier.urihttp://hdl.handle.net/10722/60340
 
dc.identifier.volume30
 
dc.languageeng
 
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/TBI
 
dc.publisher.placeSwitzerland
 
dc.relation.ispartofTumor Biology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshBase Sequence
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshDNA Methylation
 
dc.subject.meshEndometrial Neoplasms - genetics - metabolism
 
dc.subject.meshEpigenesis, Genetic
 
dc.subject.meshEstrogen Receptor alpha - genetics - metabolism
 
dc.subject.meshFemale
 
dc.subject.meshHumans
 
dc.subject.meshMetallothionein - genetics - metabolism
 
dc.subject.meshMolecular Sequence Data
 
dc.subject.meshPromoter Regions, Genetic
 
dc.subjectEndometrial carcinoma
 
dc.subjectMetallothionein 1E gene
 
dc.subjectPromoter hypermethylation
 
dc.titleEpigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas
 
dc.typeArticle
 
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<contributor.author>Tam, KF</contributor.author>
<contributor.author>Chan, KKL</contributor.author>
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Author Affiliations
  1. The University of Hong Kong