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Article: Inactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines

TitleInactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
Authors
KeywordsEsophageal squamous cell carcinoma
p16INK4a
Promoter hypermethylation
Transfection
Issue Date2004
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2004, v. 208 n. 2, p. 207-213 How to Cite?
AbstractThe inactivation mechanisms and functional role of p16INK4a in three Asian esophageal squamous cell carcinoma (ESCC) cell lines were investigated by polymerase chain reaction (PCR) amplification, DNA sequencing, methylation-specific PCR analysis, reverse transcription-PCR, Western blotting, and colony formation assays. The p16INK4a was inactivated by promoter hypermethylation in all three cell lines, a homozygous deletion of exons 2 and 3, and a frameshift deletion on exon 1, leading to transcriptional silencing or the production of mutant p16INK4a protein. Two ESCC cell lines transfected with wild type p16INK4a show significantly reduced cell growth properties. The results of the present studies support the suppressive role of p16INK4a in ESCC development. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/88708
ISSN
2014 Impact Factor: 5.621
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwong, FMen_HK
dc.contributor.authorTang, JCOen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorLung, MLen_HK
dc.date.accessioned2010-09-06T09:46:55Z-
dc.date.available2010-09-06T09:46:55Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Letters, 2004, v. 208 n. 2, p. 207-213en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88708-
dc.description.abstractThe inactivation mechanisms and functional role of p16INK4a in three Asian esophageal squamous cell carcinoma (ESCC) cell lines were investigated by polymerase chain reaction (PCR) amplification, DNA sequencing, methylation-specific PCR analysis, reverse transcription-PCR, Western blotting, and colony formation assays. The p16INK4a was inactivated by promoter hypermethylation in all three cell lines, a homozygous deletion of exons 2 and 3, and a frameshift deletion on exon 1, leading to transcriptional silencing or the production of mutant p16INK4a protein. Two ESCC cell lines transfected with wild type p16INK4a show significantly reduced cell growth properties. The results of the present studies support the suppressive role of p16INK4a in ESCC development. © 2003 Elsevier 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.subjectEsophageal squamous cell carcinomaen_HK
dc.subjectp16INK4aen_HK
dc.subjectPromoter hypermethylationen_HK
dc.subjectTransfectionen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Squamous Cell - genetics - prevention & controlen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEsophageal Neoplasms - genetics - prevention & controlen_HK
dc.subject.meshGenes, p16 - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLoss of Heterozygosityen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.titleInactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell linesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=208&issue=2&spage=207&epage=213&date=2004&atitle=Inactivation+mechanisms+and+growth+suppressive+effects+of+p16INK4a+in+Asian+esophageal+squamous+carcinoma+cell+linesen_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2003.11.017en_HK
dc.identifier.pmid15142680en_HK
dc.identifier.scopuseid_2-s2.0-2442567836en_HK
dc.identifier.hkuros87417en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2442567836&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume208en_HK
dc.identifier.issue2en_HK
dc.identifier.spage207en_HK
dc.identifier.epage213en_HK
dc.identifier.isiWOS:000221682600011-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridKwong, FM=8158557800en_HK
dc.identifier.scopusauthoridTang, JCO=14056850300en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK

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