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- Publisher Website: 10.1159/000218032
- Scopus: eid_2-s2.0-65449153636
- PMID: 19420986
- WOS: WOS:000266098000006
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Article: Epigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas
Title | Epigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas | ||||||
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Authors | |||||||
Keywords | Endometrial carcinoma Metallothionein 1E gene Promoter hypermethylation | ||||||
Issue Date | 2009 | ||||||
Publisher | S 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? | ||||||
Abstract | Aberrant 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 Identifier | http://hdl.handle.net/10722/60340 | ||||||
ISSN | 2016 Impact Factor: 3.650 2023 SCImago Journal Rankings: 0.576 | ||||||
ISI Accession Number ID |
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 Field | Value | Language |
---|---|---|
dc.contributor.author | Tse, KY | en_HK |
dc.contributor.author | Liu, VWS | en_HK |
dc.contributor.author | Chan, DW | en_HK |
dc.contributor.author | Chiu, PM | en_HK |
dc.contributor.author | Tam, KF | en_HK |
dc.contributor.author | Chan, KKL | en_HK |
dc.contributor.author | Liao, XY | en_HK |
dc.contributor.author | Cheung, ANY | en_HK |
dc.contributor.author | Ngan, HYS | en_HK |
dc.date.accessioned | 2010-05-31T04:08:40Z | - |
dc.date.available | 2010-05-31T04:08:40Z | - |
dc.date.issued | 2009 | en_HK |
dc.identifier.citation | Tumor Biology, 2009, v. 30 n. 2, p. 93-99 | en_HK |
dc.identifier.issn | 1010-4283 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/60340 | - |
dc.description.abstract | Aberrant 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.language | eng | en_HK |
dc.publisher | S Karger AG. The Journal's web site is located at http://www.karger.com/TBI | en_HK |
dc.relation.ispartof | Tumor Biology | en_HK |
dc.subject | Endometrial carcinoma | en_HK |
dc.subject | Metallothionein 1E gene | en_HK |
dc.subject | Promoter hypermethylation | en_HK |
dc.subject.mesh | Base Sequence | en_HK |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | DNA Methylation | en_HK |
dc.subject.mesh | Endometrial Neoplasms - genetics - metabolism | en_HK |
dc.subject.mesh | Epigenesis, Genetic | en_HK |
dc.subject.mesh | Estrogen Receptor alpha - genetics - metabolism | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Metallothionein - genetics - metabolism | en_HK |
dc.subject.mesh | Molecular Sequence Data | en_HK |
dc.subject.mesh | Promoter Regions, Genetic | en_HK |
dc.title | Epigenetic alteration of the metallothionein 1e gene in human endometrial carcinomas | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Liu, VWS: vwsliu@hkusua.hku.hk | en_HK |
dc.identifier.email | Chan, DW: dwchan@hku.hk | en_HK |
dc.identifier.email | Chan, KKL: kklchan@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, ANY: anycheun@hkucc.hku.hk | en_HK |
dc.identifier.email | Ngan, HYS: hysngan@hkucc.hku.hk | en_HK |
dc.identifier.authority | Liu, VWS=rp00341 | en_HK |
dc.identifier.authority | Chan, DW=rp00543 | en_HK |
dc.identifier.authority | Chan, KKL=rp00499 | en_HK |
dc.identifier.authority | Cheung, ANY=rp00542 | en_HK |
dc.identifier.authority | Ngan, HYS=rp00346 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1159/000218032 | en_HK |
dc.identifier.pmid | 19420986 | en_HK |
dc.identifier.scopus | eid_2-s2.0-65449153636 | en_HK |
dc.identifier.hkuros | 157706 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-65449153636&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 30 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 93 | en_HK |
dc.identifier.epage | 99 | en_HK |
dc.identifier.isi | WOS:000266098000006 | - |
dc.publisher.place | Switzerland | en_HK |
dc.identifier.scopusauthorid | Tse, KY=8876026900 | en_HK |
dc.identifier.scopusauthorid | Liu, VWS=7006405113 | en_HK |
dc.identifier.scopusauthorid | Chan, DW=26533900600 | en_HK |
dc.identifier.scopusauthorid | Chiu, PM=7103182596 | en_HK |
dc.identifier.scopusauthorid | Tam, KF=7201692816 | en_HK |
dc.identifier.scopusauthorid | Chan, KKL=8655666700 | en_HK |
dc.identifier.scopusauthorid | Liao, XY=7202134156 | en_HK |
dc.identifier.scopusauthorid | Cheung, ANY=54927484100 | en_HK |
dc.identifier.scopusauthorid | Ngan, HYS=34571944100 | en_HK |
dc.identifier.issnl | 1010-4283 | - |