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Article: Papillomavirus type 16 E6/E7 and human telomerase reverse transcriptase in esophageal cell immortalization and early transformation

TitlePapillomavirus type 16 E6/E7 and human telomerase reverse transcriptase in esophageal cell immortalization and early transformation
Authors
KeywordsEsophageal cancer
HPV
Telomerase
Issue Date2007
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2007, v. 245 n. 1-2, p. 184-194 How to Cite?
AbstractInfection with high-risk human papillomavirus (HPV) has been implicated in the pathogenesis of esophageal squamous cell carcinoma, and up-regulation of telomerase in esophageal adenocarcinoma. We immortalized normal esophageal epithelial cells by over-expression of the HPV16 E6/E7 and human telomerase reverse transcriptase (hTERT) genes. HPV16 E6/E7-induced immortalization was accompanied by reduced RB and p53, but increased p16 and p21, protein expression. hTERT-immortalized cells had unaffected RB and p53, but significantly decreased p16 and p21, protein expression. Aurora-A protein was also up-regulated in E6E7 immortalized cells, and to a less extent in hTERT immortalized cells. Fluorescence in situ hybridization showed that the Aurora-A gene locus was amplified in E6E7 immortalized cells, which might account in part for the Aurora-A over-expression. These molecular changes led to an abrogation of the G2 checkpoint. E6E7 and hTERT immortalized esophageal cells recapitulated many of the molecular changes observed in esophageal carcinomas, where RB and p53 are frequently down-regulated. However, down-regulation of p16 and p21 occurred frequently in esophageal cancer, owing to aberrant gene promoter methylation. We showed in the immortalized cells that aberrant methylation had not yet set in, suggesting that promoter methylation might not be necessary for cellular immortalization. In addition to supporting the role of HPV and telomerase in esophageal carcinogenesis, our cell lines may also be useful in vitro models for further studies of esophageal carcinogenesis. © 2006 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67767
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, Hen_HK
dc.contributor.authorJin, Yen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorJin, Cen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorKwong, YLen_HK
dc.date.accessioned2010-09-06T05:58:04Z-
dc.date.available2010-09-06T05:58:04Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Letters, 2007, v. 245 n. 1-2, p. 184-194en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67767-
dc.description.abstractInfection with high-risk human papillomavirus (HPV) has been implicated in the pathogenesis of esophageal squamous cell carcinoma, and up-regulation of telomerase in esophageal adenocarcinoma. We immortalized normal esophageal epithelial cells by over-expression of the HPV16 E6/E7 and human telomerase reverse transcriptase (hTERT) genes. HPV16 E6/E7-induced immortalization was accompanied by reduced RB and p53, but increased p16 and p21, protein expression. hTERT-immortalized cells had unaffected RB and p53, but significantly decreased p16 and p21, protein expression. Aurora-A protein was also up-regulated in E6E7 immortalized cells, and to a less extent in hTERT immortalized cells. Fluorescence in situ hybridization showed that the Aurora-A gene locus was amplified in E6E7 immortalized cells, which might account in part for the Aurora-A over-expression. These molecular changes led to an abrogation of the G2 checkpoint. E6E7 and hTERT immortalized esophageal cells recapitulated many of the molecular changes observed in esophageal carcinomas, where RB and p53 are frequently down-regulated. However, down-regulation of p16 and p21 occurred frequently in esophageal cancer, owing to aberrant gene promoter methylation. We showed in the immortalized cells that aberrant methylation had not yet set in, suggesting that promoter methylation might not be necessary for cellular immortalization. In addition to supporting the role of HPV and telomerase in esophageal carcinogenesis, our cell lines may also be useful in vitro models for further studies of esophageal carcinogenesis. © 2006 Elsevier 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.subjectEsophageal canceren_HK
dc.subjectHPVen_HK
dc.subjectTelomeraseen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCadherins - geneticsen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshCell Transformation, Neoplastic - geneticsen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16 - genetics - metabolismen_HK
dc.subject.meshDNA Methylationen_HK
dc.subject.meshEpithelial Cells - drug effects - metabolism - pathologyen_HK
dc.subject.meshEsophagus - cytology - metabolismen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIn Situ Hybridization, Fluorescenceen_HK
dc.subject.meshNocodazole - pharmacologyen_HK
dc.subject.meshOncogene Proteins, Viral - genetics - metabolismen_HK
dc.subject.meshPapillomavirus E7 Proteinsen_HK
dc.subject.meshProtein-Serine-Threonine Kinases - genetics - metabolismen_HK
dc.subject.meshRepressor Proteins - genetics - metabolismen_HK
dc.subject.meshTelomerase - genetics - metabolismen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Suppressor Protein p53 - genetics - metabolismen_HK
dc.subject.meshTumor Suppressor Proteins - geneticsen_HK
dc.titlePapillomavirus type 16 E6/E7 and human telomerase reverse transcriptase in esophageal cell immortalization and early transformationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=245&issue=1-2&spage=184&epage=194&date=2007&atitle=Papillomavirus+type+16+E6/E7+and+human+telomerase+reverse+transcriptase+in+esophageal+cell+immortalization+and+early+transformationen_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL: ylkwong@hku.hken_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2006.01.005en_HK
dc.identifier.pmid16488074en_HK
dc.identifier.scopuseid_2-s2.0-33845751069en_HK
dc.identifier.hkuros127265en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845751069&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume245en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage184en_HK
dc.identifier.epage194en_HK
dc.identifier.isiWOS:000244146100023-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridZhang, H=8965962000en_HK
dc.identifier.scopusauthoridJin, Y=7404457413en_HK
dc.identifier.scopusauthoridChen, X=8252513600en_HK
dc.identifier.scopusauthoridJin, C=7401659093en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK

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