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Article: Resistance to apoptosis of HPV 16-infected laryngeal cancer cells is associated with decreased Bak and increased Bcl-2 expression

TitleResistance to apoptosis of HPV 16-infected laryngeal cancer cells is associated with decreased Bak and increased Bcl-2 expression
Authors
KeywordsBak
Bcl-2
Human papillomavirus type 16
Laryngeal cancer
p53
Issue Date2004
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2004, v. 205 n. 1, p. 81-88 How to Cite?
AbstractHuman papillomavirus type 16 (HPV 16) plays an etiological role in human laryngeal carcinoma. Apoptosis is closely associated with various biological processes including oncogenesis. This study investigated how HPV 16 oncoproteins E6 and E7 affect apoptosis in human laryngeal cancer cells. We established two human laryngeal cancer cell lines that expressed HPV 16 E6 and E7, respectively. Using these two cell lines, we found that both E6 and E7 exhibited an inhibitive effect on apoptosis induced by tumor necrosis factor alpha and cycloheximide. In both transfected cell lines, the expression of pro-apoptotic Bak was reduced and that of anti-apoptotic Bcl-2 was over-expressed. However, the expression of caspase-3 and caspase-8 was not significantly different between the E6- and E7-transfected cells and the control cells without HPV 16. p53 Protein was not detected in either the transfected or the non-transfected cells. Our study indicates that: (1) HPV 16 E6 and E7 oncoproteins are capable of inhibiting apoptosis in laryngeal squamous carcinoma cells; (2) the mechanism modulated by E6 and E7 involves the over-expression of Bcl-2 and the down-regulation of Bak; (3) the anti-apoptotic pathway is not related to the level of p53, caspase-3, or caspase-8. These results suggest that the dysregulation of apoptotic molecules Bak and Bcl-2 by HPV 16 E6 and E7 plays a role in the prolongation of cell survival, which may subsequently contribute to the development of human laryngeal cancer. © 2003 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92057
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDu, Jen_HK
dc.contributor.authorChen, GGen_HK
dc.contributor.authorVlantis, ACen_HK
dc.contributor.authorChan, PKSen_HK
dc.contributor.authorTsang, RKYen_HK
dc.contributor.authorVan Hasselt, CAen_HK
dc.date.accessioned2010-09-17T10:34:49Z-
dc.date.available2010-09-17T10:34:49Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Letters, 2004, v. 205 n. 1, p. 81-88en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92057-
dc.description.abstractHuman papillomavirus type 16 (HPV 16) plays an etiological role in human laryngeal carcinoma. Apoptosis is closely associated with various biological processes including oncogenesis. This study investigated how HPV 16 oncoproteins E6 and E7 affect apoptosis in human laryngeal cancer cells. We established two human laryngeal cancer cell lines that expressed HPV 16 E6 and E7, respectively. Using these two cell lines, we found that both E6 and E7 exhibited an inhibitive effect on apoptosis induced by tumor necrosis factor alpha and cycloheximide. In both transfected cell lines, the expression of pro-apoptotic Bak was reduced and that of anti-apoptotic Bcl-2 was over-expressed. However, the expression of caspase-3 and caspase-8 was not significantly different between the E6- and E7-transfected cells and the control cells without HPV 16. p53 Protein was not detected in either the transfected or the non-transfected cells. Our study indicates that: (1) HPV 16 E6 and E7 oncoproteins are capable of inhibiting apoptosis in laryngeal squamous carcinoma cells; (2) the mechanism modulated by E6 and E7 involves the over-expression of Bcl-2 and the down-regulation of Bak; (3) the anti-apoptotic pathway is not related to the level of p53, caspase-3, or caspase-8. These results suggest that the dysregulation of apoptotic molecules Bak and Bcl-2 by HPV 16 E6 and E7 plays a role in the prolongation of cell survival, which may subsequently contribute to the development of human laryngeal cancer. © 2003 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
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.subjectBaken_HK
dc.subjectBcl-2en_HK
dc.subjectHuman papillomavirus type 16en_HK
dc.subjectLaryngeal canceren_HK
dc.subjectp53en_HK
dc.titleResistance to apoptosis of HPV 16-infected laryngeal cancer cells is associated with decreased Bak and increased Bcl-2 expressionen_HK
dc.typeArticleen_HK
dc.identifier.emailTsang, RKY: rkytsang@hku.hken_HK
dc.identifier.authorityTsang, RKY=rp01386en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2003.09.035en_HK
dc.identifier.pmid15036664-
dc.identifier.scopuseid_2-s2.0-1242293656en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1242293656&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume205en_HK
dc.identifier.issue1en_HK
dc.identifier.spage81en_HK
dc.identifier.epage88en_HK
dc.identifier.isiWOS:000220035800011-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridDu, J=36837684600en_HK
dc.identifier.scopusauthoridChen, GG=35291566400en_HK
dc.identifier.scopusauthoridVlantis, AC=35585515400en_HK
dc.identifier.scopusauthoridChan, PKS=7403497792en_HK
dc.identifier.scopusauthoridTsang, RKY=7102940058en_HK
dc.identifier.scopusauthoridVan Hasselt, CA=7103394173en_HK

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