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Conference Paper: The role of Id-1 in immortalization of esophageal epithelial cells

TitleThe role of Id-1 in immortalization of esophageal epithelial cells
Authors
Issue Date2006
PublisherAmerican Association for Cancer Research
Citation
The 97th American Association for Cancer Research Annual Meeting, Washington, DC, 1-5 April 2006. In Cancer Research, 2006, v. 66 n. 8S, p. 1003 Abstract no. 4271 How to Cite?
AbstractThe potential to achieve limitless proliferation is one of the major hallmarks of cancer. Identifying the molecular basis responsible for regulating the replicative potential has important implications for carcinogenesis. It is well documented that the introduction of hTERT, the catalytic subunit of telomerase helps to overcome replicative senescence and acquire immortality. Recently, it has been reported that ectopic expression of Id-1 (Inhibitor of Differentiation), a helix-loop-helix protein which serves as a negative regulator in the regulation of transcription and differentiation, also leads to delayed senescence and even immortalization of human keratinocytes through activation of telomerase. On the other hand, human embryonic fibroblasts transfected with hTERT exhibit increased Id-1 expression. In this study, the role of Id-1 and its relationship with hTERT in immortalization of human esophageal epithelial cells was investigated by overexpressing Id-1 or hTERT, or both Id-1 and hTERT, in esophageal epithelial primary cell lines. Our results showed that in an hTERT-immortalized esophageal cell line, NE083, the expression of Id-1 increased with increasing passages. Knockdown of endogenous Id-1 at late passage (P35) by transfection with antisense Id-1 led to suppressed cell growth, down-regulation of Mdm2 and increased sensitivity to TGF-β-induced differentiation and growth arrest. In another hTERT-transfected primary esophageal cell line, NE2, cells transfected with Id-1 showed elevated growth rate, up-regulation of pMdm2 and down-regulation of p21, compared with cells without Id-1 transfected. These findings suggested that Id-1 may induce proliferation of esophageal epithelial cells and help hTERT promoting immortalization of esophageal epithelial cells, possibly through regulating the p21Waf/Cip/Mdm2 pathway.
Persistent Identifierhttp://hdl.handle.net/10722/95171
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorCheung, PYen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorCheung, Aen_HK
dc.date.accessioned2010-09-25T15:53:52Z-
dc.date.available2010-09-25T15:53:52Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 97th American Association for Cancer Research Annual Meeting, Washington, DC, 1-5 April 2006. In Cancer Research, 2006, v. 66 n. 8S, p. 1003 Abstract no. 4271en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95171-
dc.description.abstractThe potential to achieve limitless proliferation is one of the major hallmarks of cancer. Identifying the molecular basis responsible for regulating the replicative potential has important implications for carcinogenesis. It is well documented that the introduction of hTERT, the catalytic subunit of telomerase helps to overcome replicative senescence and acquire immortality. Recently, it has been reported that ectopic expression of Id-1 (Inhibitor of Differentiation), a helix-loop-helix protein which serves as a negative regulator in the regulation of transcription and differentiation, also leads to delayed senescence and even immortalization of human keratinocytes through activation of telomerase. On the other hand, human embryonic fibroblasts transfected with hTERT exhibit increased Id-1 expression. In this study, the role of Id-1 and its relationship with hTERT in immortalization of human esophageal epithelial cells was investigated by overexpressing Id-1 or hTERT, or both Id-1 and hTERT, in esophageal epithelial primary cell lines. Our results showed that in an hTERT-immortalized esophageal cell line, NE083, the expression of Id-1 increased with increasing passages. Knockdown of endogenous Id-1 at late passage (P35) by transfection with antisense Id-1 led to suppressed cell growth, down-regulation of Mdm2 and increased sensitivity to TGF-β-induced differentiation and growth arrest. In another hTERT-transfected primary esophageal cell line, NE2, cells transfected with Id-1 showed elevated growth rate, up-regulation of pMdm2 and down-regulation of p21, compared with cells without Id-1 transfected. These findings suggested that Id-1 may induce proliferation of esophageal epithelial cells and help hTERT promoting immortalization of esophageal epithelial cells, possibly through regulating the p21Waf/Cip/Mdm2 pathway.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleThe role of Id-1 in immortalization of esophageal epithelial cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailCheung, A: lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.hkuros115267en_HK

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