File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Inactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
  • Basic View
  • Metadata View
  • XML View
TitleInactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
 
AuthorsKwong, FM3
Tang, JCO2 1
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
2012 Impact Factor: 4.258
2012 SCImago Journal Rankings: 1.502
 
DOIhttp://dx.doi.org/10.1016/j.canlet.2003.11.017
 
ISI Accession Number IDWOS:000221682600011
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2012 Impact Factor: 4.258
2012 SCImago Journal Rankings: 1.502
 
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
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Kwong, FM</contributor.author>
<contributor.author>Tang, JCO</contributor.author>
<contributor.author>Srivastava, G</contributor.author>
<contributor.author>Lung, ML</contributor.author>
<date.accessioned>2010-09-06T09:46:55Z</date.accessioned>
<date.available>2010-09-06T09:46:55Z</date.available>
<date.issued>2004</date.issued>
<identifier.citation>Cancer Letters, 2004, v. 208 n. 2, p. 207-213</identifier.citation>
<identifier.issn>0304-3835</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/88708</identifier.uri>
<description.abstract>The 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. &#169; 2003 Elsevier Ltd. All rights reserved.</description.abstract>
<language>eng</language>
<publisher>Elsevier Ireland Ltd. The Journal&apos;s web site is located at http://www.elsevier.com/locate/canlet</publisher>
<relation.ispartof>Cancer Letters</relation.ispartof>
<rights>Cancer Letters. Copyright &#169; Elsevier Ireland Ltd.</rights>
<subject>Esophageal squamous cell carcinoma</subject>
<subject>p16INK4a</subject>
<subject>Promoter hypermethylation</subject>
<subject>Transfection</subject>
<subject.mesh>Blotting, Western</subject.mesh>
<subject.mesh>Carcinoma, Squamous Cell - genetics - prevention &amp; control</subject.mesh>
<subject.mesh>Cell Line, Tumor</subject.mesh>
<subject.mesh>DNA Methylation</subject.mesh>
<subject.mesh>Esophageal Neoplasms - genetics - prevention &amp; control</subject.mesh>
<subject.mesh>Genes, p16 - physiology</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Loss of Heterozygosity</subject.mesh>
<subject.mesh>Polymerase Chain Reaction</subject.mesh>
<title>Inactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0304-3835&amp;volume=208&amp;issue=2&amp;spage=207&amp;epage=213&amp;date=2004&amp;atitle=Inactivation+mechanisms+and+growth+suppressive+effects+of+p16INK4a+in+Asian+esophageal+squamous+carcinoma+cell+lines</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/j.canlet.2003.11.017</identifier.doi>
<identifier.pmid>15142680</identifier.pmid>
<identifier.scopus>eid_2-s2.0-2442567836</identifier.scopus>
<identifier.hkuros>87417</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-2442567836&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>208</identifier.volume>
<identifier.issue>2</identifier.issue>
<identifier.spage>207</identifier.spage>
<identifier.epage>213</identifier.epage>
<identifier.isi>WOS:000221682600011</identifier.isi>
<publisher.place>Ireland</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. Hong Kong Polytechnic University
  3. Hong Kong University of Science and Technology