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Article: E-cadherin expression is commonly downregulated by CpG island hypermethylation in esophageal carcinoma cells

TitleE-cadherin expression is commonly downregulated by CpG island hypermethylation in esophageal carcinoma cells
Authors
KeywordsCpG island methylation
E-Cadherin
Esophageal carcinoma
Issue Date2001
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2001, v. 173 n. 1, p. 71-78 How to Cite?
AbstractE-cadherin, a cell adhesion molecule, is regarded as an invasion-suppressor molecule and a prognostic marker in many types of human cancers. Downregulation of E-cadherin is common in esophageal carcinoma and is associated with an increase in invasive and metastatic potential. To study the mechanisms responsible for inactivation of this gene in esophageal squamous cell carcinoma (ESCC), we investigated the methylation status around the 5′ promoter region of E-cadherin gene of six ESCC cell lines by methylation-specific polymerase chain reaction, and compared it with E-cadherin protein and mRNA expression. We also studied the methylation status of 20 ESCC clinical specimens. Methylation was noted in four of the six cell lines (one fully methylated and three partially methylated). The completely methylated cell line lacked E-cadherin protein expression and mRNA transcription. E-cadherin expression and transcription were reduced in a partially methylated cell line but preserved in the other partially methylated cell lines. Treatment of E-cadherin-negative carcinoma cells with the demethylating agent, 5-aza-2′-deoxycytidine, induced re-expression of the gene. A high frequency of methylation (16/20, 80%) was also noted in the 20 ESCC clinical samples. Our results indicate that 5′ CpG island methylation is common in esophageal carcinoma and may play an important role in downregulation of E-cadherin. © 2001 Elsevier Science Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67959
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSi, HXen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorLam, KYen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorShen, ZYen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:59:49Z-
dc.date.available2010-09-06T05:59:49Z-
dc.date.issued2001en_HK
dc.identifier.citationCancer Letters, 2001, v. 173 n. 1, p. 71-78en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67959-
dc.description.abstractE-cadherin, a cell adhesion molecule, is regarded as an invasion-suppressor molecule and a prognostic marker in many types of human cancers. Downregulation of E-cadherin is common in esophageal carcinoma and is associated with an increase in invasive and metastatic potential. To study the mechanisms responsible for inactivation of this gene in esophageal squamous cell carcinoma (ESCC), we investigated the methylation status around the 5′ promoter region of E-cadherin gene of six ESCC cell lines by methylation-specific polymerase chain reaction, and compared it with E-cadherin protein and mRNA expression. We also studied the methylation status of 20 ESCC clinical specimens. Methylation was noted in four of the six cell lines (one fully methylated and three partially methylated). The completely methylated cell line lacked E-cadherin protein expression and mRNA transcription. E-cadherin expression and transcription were reduced in a partially methylated cell line but preserved in the other partially methylated cell lines. Treatment of E-cadherin-negative carcinoma cells with the demethylating agent, 5-aza-2′-deoxycytidine, induced re-expression of the gene. A high frequency of methylation (16/20, 80%) was also noted in the 20 ESCC clinical samples. Our results indicate that 5′ CpG island methylation is common in esophageal carcinoma and may play an important role in downregulation of E-cadherin. © 2001 Elsevier Science Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectCpG island methylationen_HK
dc.subjectE-Cadherinen_HK
dc.subjectEsophageal carcinomaen_HK
dc.subject.meshAzacitidine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshCadherins - biosynthesis - geneticsen_HK
dc.subject.meshCarcinoma - genetics - metabolismen_HK
dc.subject.meshCpG Islandsen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshDNA Modification Methylases - antagonists & inhibitorsen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshEsophageal Neoplasms - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshRNA, Neoplasm - biosynthesisen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.titleE-cadherin expression is commonly downregulated by CpG island hypermethylation in esophageal carcinoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=173&spage=71&epage=78&date=2001&atitle=E-cadherin+expression+is+commonly+downregulated+by+CpG+island+hypermethylation+in+esophageal+carcinoma+cellsen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0304-3835(01)00646-2en_HK
dc.identifier.pmid11578811-
dc.identifier.scopuseid_2-s2.0-0035829016en_HK
dc.identifier.hkuros63384en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035829016&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume173en_HK
dc.identifier.issue1en_HK
dc.identifier.spage71en_HK
dc.identifier.epage78en_HK
dc.identifier.isiWOS:000171579300010-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridSi, HX=36780537100en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridLam, KY=7403657165en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridLiu, Y=26643293600en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridShen, ZY=15746894500en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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