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Conference Paper: Functional study of the EBV encoded LMP1

TitleFunctional study of the EBV encoded LMP1
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 99th Annual Meeting of the American Association of Cancer Research (AACR 2008), San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68, p. 601 How to Cite?
AbstractThe Epstein-Barr virus encoded LMP1 is expressed in nasopharyngeal caricinoma cells. Recently, we have showed that LMP1 expression in immortalized epithelial cells could induce mitotic abnormality by downregulating RASSF1A expression. Downregulation of RASSF1A affects the stability of microtubules and induces formation of abnormal spindle. Expression of LMP1 could induce many pathologic phenotypes in cells. Expression of LMP1 induces upregulation of IL6 expression to activate STAT3 signaling which may mediate the pathologic properties of nasopharyngeal carcinoma cells. LMP1 expression in immortalized nasopharyngeal epithelial cells induces malignantly transformated phenotype including anchorage independent growth in soft agar, increase of invasive properties and activation of intracellular signaling for cell survival and anti-apoptosis. LMP1 expression also suppresses the exprssion of squamous differentitation marker, p63 and other differentation properties in immortalized epithelial cells. Recently, we have showed that LMP1 could also facilitate immortalization of primary cultures of nasopharyngeal epithelial cells. LMP1 immortalized nasopharyngeal epithelial cells have upregulated MAPK signaling pathways and overexpression of EGFR.
Persistent Identifierhttp://hdl.handle.net/10722/95077
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468

 

DC FieldValueLanguage
dc.contributor.authorTsao, GSW-
dc.contributor.authorMan, CWY-
dc.contributor.authorYip, YL-
dc.contributor.authorTsang, CM-
dc.contributor.authorHau, PM-
dc.date.accessioned2010-09-25T15:50:56Z-
dc.date.available2010-09-25T15:50:56Z-
dc.date.issued2008-
dc.identifier.citationThe 99th Annual Meeting of the American Association of Cancer Research (AACR 2008), San Diego, CA, 12-16 April 2008. In Cancer Research, 2008, v. 68, p. 601-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95077-
dc.description.abstractThe Epstein-Barr virus encoded LMP1 is expressed in nasopharyngeal caricinoma cells. Recently, we have showed that LMP1 expression in immortalized epithelial cells could induce mitotic abnormality by downregulating RASSF1A expression. Downregulation of RASSF1A affects the stability of microtubules and induces formation of abnormal spindle. Expression of LMP1 could induce many pathologic phenotypes in cells. Expression of LMP1 induces upregulation of IL6 expression to activate STAT3 signaling which may mediate the pathologic properties of nasopharyngeal carcinoma cells. LMP1 expression in immortalized nasopharyngeal epithelial cells induces malignantly transformated phenotype including anchorage independent growth in soft agar, increase of invasive properties and activation of intracellular signaling for cell survival and anti-apoptosis. LMP1 expression also suppresses the exprssion of squamous differentitation marker, p63 and other differentation properties in immortalized epithelial cells. Recently, we have showed that LMP1 could also facilitate immortalization of primary cultures of nasopharyngeal epithelial cells. LMP1 immortalized nasopharyngeal epithelial cells have upregulated MAPK signaling pathways and overexpression of EGFR.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.titleFunctional study of the EBV encoded LMP1-
dc.typeConference_Paper-
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hk-
dc.identifier.emailMan, CWY: cornman@hkucc.hku.hk-
dc.identifier.emailYip, YL: elaineyip@graduate.hku.hk-
dc.identifier.emailTsang, CM: anna0226@graduate.hku.hk-
dc.identifier.emailHau, PM: tomhau10@HKUCC-COM.hku.hk-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityTsang, CM=rp01964-
dc.identifier.hkuros160586-
dc.identifier.volume68-
dc.identifier.spage601-
dc.identifier.epage601-
dc.publisher.placeUnited States-
dc.identifier.issnl0008-5472-

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