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Conference Paper: Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) regulates the expression of p63 in immortalized epithelial cells

TitleEpstein-Barr virus (EBV) latent membrane protein 1 (LMP1) regulates the expression of p63 in immortalized epithelial cells
Authors
Issue Date2009
PublisherAmerican Association of Cancer Research.
Citation
The 100th Annual Meeting of the American Association of Cancer Research (AACR 2009), Denver, CO., 18-22 April 2009. How to Cite?
AbstractThe present study aims at studying the mechanism on how EBV promotes carcinogenesis by altering the p63 pathways. p63, a family member of p53, is involved in cancer and epidermal development. Due to different promoters usage and alternative splicing at the 3’ end of the transcripts, there exists different p63 isoforms. Among them, the ΔNp63α is the predominant form in epithelial cells. Emerging evidence has shown that ΔNp63α is involved in controlling proliferation, apoptosis and metastasis in cancer cells. Epidermal development requires a balance between cell proliferation and differentiation. It has been demonstrated that p63 is a “master gene” in regulating this process since p63 knockout mice fail to develop normal stratified epidermis while ΔNp63α plays an essential role in this developmental process. EBV is well known to inhibit cell differentiation, and LMP1 is thought to be closely linked to this process. Here we show that exogenous LMP1 downregulates p63 in established keratinocytes cell lines and immortalized nasopharyngeal epithelial cell lines. The alteration of p63 level may be related to decrease in protein stability since p63 transcript level remains unchanged as demonstrated in RT-PCR experiment. Furthermore, LMP1 expression causes translocation of p63 from nucleus to cytoplasm as shown by immunofluorescence experiment using antibody that targets endogenous p63. Future works will focus on the mechanisms of LMP1 in promoting the degradation of p63. And this work may help to elucidate how LMP1 drives epithelial cell transformation via the p63 pathways.
DescriptionPoster Presentations - Pathogen-Host Interaction and Transformation: abstract no. 781
Persistent Identifierhttp://hdl.handle.net/10722/135778

 

DC FieldValueLanguage
dc.contributor.authorHau, PMen_US
dc.contributor.authorTsao, GSWen_US
dc.date.accessioned2011-07-27T01:48:03Z-
dc.date.available2011-07-27T01:48:03Z-
dc.date.issued2009en_US
dc.identifier.citationThe 100th Annual Meeting of the American Association of Cancer Research (AACR 2009), Denver, CO., 18-22 April 2009.en_US
dc.identifier.urihttp://hdl.handle.net/10722/135778-
dc.descriptionPoster Presentations - Pathogen-Host Interaction and Transformation: abstract no. 781-
dc.description.abstractThe present study aims at studying the mechanism on how EBV promotes carcinogenesis by altering the p63 pathways. p63, a family member of p53, is involved in cancer and epidermal development. Due to different promoters usage and alternative splicing at the 3’ end of the transcripts, there exists different p63 isoforms. Among them, the ΔNp63α is the predominant form in epithelial cells. Emerging evidence has shown that ΔNp63α is involved in controlling proliferation, apoptosis and metastasis in cancer cells. Epidermal development requires a balance between cell proliferation and differentiation. It has been demonstrated that p63 is a “master gene” in regulating this process since p63 knockout mice fail to develop normal stratified epidermis while ΔNp63α plays an essential role in this developmental process. EBV is well known to inhibit cell differentiation, and LMP1 is thought to be closely linked to this process. Here we show that exogenous LMP1 downregulates p63 in established keratinocytes cell lines and immortalized nasopharyngeal epithelial cell lines. The alteration of p63 level may be related to decrease in protein stability since p63 transcript level remains unchanged as demonstrated in RT-PCR experiment. Furthermore, LMP1 expression causes translocation of p63 from nucleus to cytoplasm as shown by immunofluorescence experiment using antibody that targets endogenous p63. Future works will focus on the mechanisms of LMP1 in promoting the degradation of p63. And this work may help to elucidate how LMP1 drives epithelial cell transformation via the p63 pathways.-
dc.languageengen_US
dc.publisherAmerican Association of Cancer Research.-
dc.relation.ispartofProceedings of American Association of Cancer Research, 2009en_US
dc.titleEpstein-Barr virus (EBV) latent membrane protein 1 (LMP1) regulates the expression of p63 in immortalized epithelial cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailHau, PM: tomhau10@hku.hken_US
dc.identifier.emailTsao, GSW: gswtsao@hku.hken_US
dc.identifier.authorityTsao, GSW=rp00399en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros186961en_US
dc.publisher.placeUnited States-
dc.description.otherThe 100th Annual Meeting of the American Association of Cancer Research (AACR 2009), Denver, CO., 18-22 April 2009.-

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