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Article: Regulation of p63 expression in primary and immortalized nasopharyngeal epithelial cells

TitleRegulation of p63 expression in primary and immortalized nasopharyngeal epithelial cells
Authors
Issue Date2008
PublisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/
Citation
International Journal Of Oncology, 2008, v. 33 n. 4, p. 713-724 How to Cite?
AbstractMutation of the p53 gene is a common event in human cancer. Interestingly, p53 mutation is uncommon in nasopharyngeal carcinoma (NPC). The ΔNp63 has been postulated to have a dominant-negative effect on the function of the p53 gene and may play a role in the pathogenesis of nasopharyngeal carcinoma. Immortalization is a common property of cancer cells and is believed to be an early event in carcinogenesis. At present, the relationship between ΔNp63 and immortalization is poorly understood. In this study, we defined the expression profile of p63 and its various isoforms in primary and immortalized nasopharyngeal epithelial cells. Also, we elucidated some events regulating the expression of p63. Elevated expression of p63 was generally detected in both primary and immortalized nasopharyngeal epithelial cells at their proliferation stage and the predominant isoform of p63 expressed was ΔNp63α. p63 expression was suppressed upon cellular senescence of primary nasopharyngeal epithelial cells and induction of terminal differentiation in immortalized nasopharyngeal epithelial cells. Expression of ΔNp63 alone was able to drive clonal proliferation in primary nasopharyngeal cells in culture while downregulation of ΔNp63 induced cellular apoptosis. All these results support a role of ΔNp63 in proliferation and immortalization which facilitates pathogenesis of nasopharyngeal carcinoma. TGFβ and retinoic acid downregulated the expression of p63 in immortalized nasopharyngeal epithelial cells and may play a role in regulating differentiation in squamous epithelial cells with potential applications in prevention and treatment of nasopharyngeal carcinoma.
Persistent Identifierhttp://hdl.handle.net/10722/58179
ISSN
2015 Impact Factor: 3.018
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council, Hong KongHKU7457/04M
University of Hong Kong
Funding Information:

This study was sponsored by the funding support received from the Research Grants Council, Hong Kong (HKU7457/04M), and a CRCG grant received from the University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorYip, YLen_HK
dc.contributor.authorTsao, GSWen_HK
dc.date.accessioned2010-05-31T03:25:17Z-
dc.date.available2010-05-31T03:25:17Z-
dc.date.issued2008en_HK
dc.identifier.citationInternational Journal Of Oncology, 2008, v. 33 n. 4, p. 713-724en_HK
dc.identifier.issn1019-6439en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58179-
dc.description.abstractMutation of the p53 gene is a common event in human cancer. Interestingly, p53 mutation is uncommon in nasopharyngeal carcinoma (NPC). The ΔNp63 has been postulated to have a dominant-negative effect on the function of the p53 gene and may play a role in the pathogenesis of nasopharyngeal carcinoma. Immortalization is a common property of cancer cells and is believed to be an early event in carcinogenesis. At present, the relationship between ΔNp63 and immortalization is poorly understood. In this study, we defined the expression profile of p63 and its various isoforms in primary and immortalized nasopharyngeal epithelial cells. Also, we elucidated some events regulating the expression of p63. Elevated expression of p63 was generally detected in both primary and immortalized nasopharyngeal epithelial cells at their proliferation stage and the predominant isoform of p63 expressed was ΔNp63α. p63 expression was suppressed upon cellular senescence of primary nasopharyngeal epithelial cells and induction of terminal differentiation in immortalized nasopharyngeal epithelial cells. Expression of ΔNp63 alone was able to drive clonal proliferation in primary nasopharyngeal cells in culture while downregulation of ΔNp63 induced cellular apoptosis. All these results support a role of ΔNp63 in proliferation and immortalization which facilitates pathogenesis of nasopharyngeal carcinoma. TGFβ and retinoic acid downregulated the expression of p63 in immortalized nasopharyngeal epithelial cells and may play a role in regulating differentiation in squamous epithelial cells with potential applications in prevention and treatment of nasopharyngeal carcinoma.en_HK
dc.languageengen_HK
dc.publisherSpandidos Publications. The Journal's web site is located at http://www.spandidos-publications.com/ijo/en_HK
dc.relation.ispartofInternational Journal of Oncologyen_HK
dc.subject.meshCarcinoma, Squamous Cell - drug therapy - pathologyen_HK
dc.subject.meshCell Agingen_HK
dc.subject.meshCell Lineen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshDNA, Complementary - metabolismen_HK
dc.subject.meshEpithelial Cells - drug effects - metabolismen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshModels, Biologicalen_HK
dc.subject.meshMutationen_HK
dc.subject.meshNasopharyngeal Neoplasms - drug therapyen_HK
dc.subject.meshRNA - metabolismen_HK
dc.subject.meshRetroviridae - geneticsen_HK
dc.subject.meshTrans-Activators - metabolismen_HK
dc.subject.meshTranscription Factorsen_HK
dc.subject.meshTransforming Growth Factor beta1 - metabolismen_HK
dc.subject.meshTumor Suppressor Proteins - metabolismen_HK
dc.titleRegulation of p63 expression in primary and immortalized nasopharyngeal epithelial cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1019-6439&volume=33&spage=713&epage=724&date=2008&atitle=Regulation+of+p63+expression+in+primary+and+immortalized+nasopharyngeal+epithelial+cellsen_HK
dc.identifier.emailTsao, GSW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.3892/ijo_00000057en_HK
dc.identifier.pmid18813784-
dc.identifier.scopuseid_2-s2.0-54049083811en_HK
dc.identifier.hkuros160584en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54049083811&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume33en_HK
dc.identifier.issue4en_HK
dc.identifier.spage713en_HK
dc.identifier.epage724en_HK
dc.identifier.isiWOS:000259769400010-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridYip, YL=7005596403en_HK
dc.identifier.scopusauthoridTsao, GSW=7102813116en_HK

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