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Article: Genetic alterations in a telomerase-immortalized human esophageal epithelial cell line: Implications for carcinogenesis

TitleGenetic alterations in a telomerase-immortalized human esophageal epithelial cell line: Implications for carcinogenesis
Authors
KeywordsEsophageal
Immortalization
Karyotype
P16 INK4a
Telomerase
Issue Date2010
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2010, v. 293 n. 1, p. 41-51 How to Cite?
AbstractEctopic expression of viral oncoproteins disrupts cellular functions and limits the value of many existing immortalization models as models for carcinogenesis, especially for cancers without definitive viral etiology. Our newly established telomerase-immortalized human esophageal epithelial cell line, NE2-hTERT, retained nearly-diploid and non-tumorigenic characteristics, but exhibited genetic and genomic alterations commonly found in esophageal cancer, including progressive loss of the p16 INK4a alleles, upregulation of anti-apoptotic proteins, epithelial-mesenchymal transition, whole-chromosome 7 gain and duplicated 5q arm. Our data also revealed a novel positive regulation of p16 INK4a on cyclin D1. These findings probably represent early crucial events and mechanisms in esophageal carcinogenesis. © 2009 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/138948
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
Funding AgencyGrant Number
Council of Hong Kong Special Administrative Region, ChinaHKU 7556/06M
HKUST 2/06C
Funding Information:

We thank Alla Li, Tony Chan, Tom Hau and Liang Hu for technical assistance; and Department of Pediatrics and Adolescent Medicine, The University of Hong Kong, for use of SKY facilities. This study was supported by a General Research Fund (Project No. HKU 7556/06M) and a Collaborative Research Fund (Project No. HKUST 2/06C) from the Research Grants Council of Hong Kong Special Administrative Region, China.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorCheung, PYen_HK
dc.contributor.authorDeng, Wen_HK
dc.contributor.authorMan, Cen_HK
dc.contributor.authorTse, WWen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2011-09-23T05:42:48Z-
dc.date.available2011-09-23T05:42:48Z-
dc.date.issued2010en_HK
dc.identifier.citationCancer Letters, 2010, v. 293 n. 1, p. 41-51en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138948-
dc.description.abstractEctopic expression of viral oncoproteins disrupts cellular functions and limits the value of many existing immortalization models as models for carcinogenesis, especially for cancers without definitive viral etiology. Our newly established telomerase-immortalized human esophageal epithelial cell line, NE2-hTERT, retained nearly-diploid and non-tumorigenic characteristics, but exhibited genetic and genomic alterations commonly found in esophageal cancer, including progressive loss of the p16 INK4a alleles, upregulation of anti-apoptotic proteins, epithelial-mesenchymal transition, whole-chromosome 7 gain and duplicated 5q arm. Our data also revealed a novel positive regulation of p16 INK4a on cyclin D1. These findings probably represent early crucial events and mechanisms in esophageal carcinogenesis. © 2009 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
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.subjectEsophagealen_HK
dc.subjectImmortalizationen_HK
dc.subjectKaryotypeen_HK
dc.subjectP16 INK4aen_HK
dc.subjectTelomeraseen_HK
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolism - pathology-
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathology-
dc.subject.meshEsophagus - metabolism - pathology - physiology-
dc.subject.meshNeoplasms, Squamous Cell - genetics - metabolism - pathology-
dc.subject.meshTelomerase - biosynthesis - genetics-
dc.titleGenetic alterations in a telomerase-immortalized human esophageal epithelial cell line: Implications for carcinogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=293&issue=1&spage=41&epage=51&date=2010&atitle=Genetic+alterations+in+a+telomerase-immortalized+human+esophageal+epithelial+cell+line:+implications+for+carcinogenesis-
dc.identifier.emailDeng, W: wdeng@hkucc.hku.hken_HK
dc.identifier.emailSrivastava, G: sgopesh@hkucc.hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hku.hken_HK
dc.identifier.emailCheung, ALM: lmcheung@hku.hken_HK
dc.identifier.authorityDeng, W=rp01640en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2009.12.015en_HK
dc.identifier.pmid20092939-
dc.identifier.scopuseid_2-s2.0-77952424612en_HK
dc.identifier.hkuros170561en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952424612&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume293en_HK
dc.identifier.issue1en_HK
dc.identifier.spage41en_HK
dc.identifier.epage51en_HK
dc.identifier.isiWOS:000278155900005-
dc.publisher.placeIrelanden_HK
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectCentromeric instability in human cells undergoing immortalization: implication for progression of chromosomal instability in carcinogenesis-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridCheung, PY=14024149900en_HK
dc.identifier.scopusauthoridDeng, W=7202223673en_HK
dc.identifier.scopusauthoridMan, C=7005722377en_HK
dc.identifier.scopusauthoridTse, WW=36495668600en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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