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

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TitleInactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
AuthorsKwong, FM3
Tang, JCO1 2
Srivastava, G1
Lung, ML3
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
CitationCancer Letters, 2004, v. 208 n. 2, p. 207-213 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.canlet.2003.11.017
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.
ISSN0304-3835
2011 Impact Factor: 4.238
2011 SCImago Journal Rankings: 0.494
DOIhttp://dx.doi.org/10.1016/j.canlet.2003.11.017
ISI Accession Number IDWOS:000221682600011
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorKwong, FM
dc.contributor.authorTang, JCO
dc.contributor.authorSrivastava, G
dc.contributor.authorLung, ML
dc.date.accessioned2010-09-06T09:46:55Z
dc.date.available2010-09-06T09:46:55Z
dc.date.issued2004
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCancer Letters, 2004, v. 208 n. 2, p. 207-213 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.canlet.2003.11.017
dc.identifier.doihttp://dx.doi.org/10.1016/j.canlet.2003.11.017
dc.identifier.epage213
dc.identifier.hkuros87417
dc.identifier.isiWOS:000221682600011
dc.identifier.issn0304-3835
2011 Impact Factor: 4.238
2011 SCImago Journal Rankings: 0.494
dc.identifier.issue2
dc.identifier.openurl
dc.identifier.pmid15142680
dc.identifier.scopuseid_2-s2.0-2442567836
dc.identifier.spage207
dc.identifier.urihttp://hdl.handle.net/10722/88708
dc.identifier.volume208
dc.languageeng
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
dc.publisher.placeIreland
dc.relation.ispartofCancer Letters
dc.relation.referencesReferences in Scopus
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.
dc.subject.meshBlotting, Western
dc.subject.meshCarcinoma, Squamous Cell - genetics - prevention & control
dc.subject.meshCell Line, Tumor
dc.subject.meshDNA Methylation
dc.subject.meshEsophageal Neoplasms - genetics - prevention & control
dc.subject.meshGenes, p16 - physiology
dc.subject.meshHumans
dc.subject.meshLoss of Heterozygosity
dc.subject.meshPolymerase Chain Reaction
dc.subjectEsophageal squamous cell carcinoma
dc.subjectp16INK4a
dc.subjectPromoter hypermethylation
dc.subjectTransfection
dc.titleInactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Hong Kong Polytechnic University
  3. Hong Kong University of Science and Technology