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Article: O-032. the relationship of p85 and the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)

TitleO-032. the relationship of p85 and the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)
Authors
Issue Date2001
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/oraloncology
Citation
Oral Oncology, 2001, v. 37 SUPPL. 1, p. S25 How to Cite?
AbstractAims: The synthetic retinoid, N-(4-Hydroxyphenyl)retinamide (4HPR), is a candidate drug for cancer treatment due to its demonstrated ability to induce apoptosis in many tumor cell lines. To further evaluate its usefulness as a chemopreventive agent, we investigated the basic mechanism of its action by examining the effect on the expression of p85-protein, a regulatory subunit of phosphatidylinositol (PI) 3-kinases known to be a regulator of apoptosis. Methods: The cultured CNE3 epithelial tumor cells established from a poorly differentiated nasopharyngeal carcinoma were used in the present study. The expression of p85 was measured by Western Blotting. Apoptosis was assessed with fluorescence microscopy, DNA fragmentation assay, flow-cytometric analysis and caspase-3 cleavage. Results: Treatment of the CNE3 cells with 4HPR dose-dependently induced apoptosis as well as an elevation in the protein level of p85. The increased expression could be detected after 12 h of incubation with 4HPR at a concentration of 5 μM, and lasted for as long as 4HPR was present. A similar observation was made in another head and neck tumor derived cell line AC3. Inhibition of PI 3-kinases activity by the specific inhibitor LY294002 enhanced 4HPR-induced apoptosis, as detected by flow-cytometry and the increased cleavage of caspase-3. Conclusion: This study demonstrated that the expression of p85 was upregulated in response to 4HPR and suggests that the increased expression of p85 is likely to play a role other than in the activation of PI 3-kinases, which would protect the CNE3 cells against apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/147542
ISSN
2015 Impact Factor: 4.286
2015 SCImago Journal Rankings: 1.764

 

DC FieldValueLanguage
dc.contributor.authorXia, Yen_US
dc.contributor.authorWong, NSen_US
dc.contributor.authorTideman, Hen_US
dc.date.accessioned2012-05-29T06:04:28Z-
dc.date.available2012-05-29T06:04:28Z-
dc.date.issued2001en_US
dc.identifier.citationOral Oncology, 2001, v. 37 SUPPL. 1, p. S25en_US
dc.identifier.issn1368-8375en_US
dc.identifier.urihttp://hdl.handle.net/10722/147542-
dc.description.abstractAims: The synthetic retinoid, N-(4-Hydroxyphenyl)retinamide (4HPR), is a candidate drug for cancer treatment due to its demonstrated ability to induce apoptosis in many tumor cell lines. To further evaluate its usefulness as a chemopreventive agent, we investigated the basic mechanism of its action by examining the effect on the expression of p85-protein, a regulatory subunit of phosphatidylinositol (PI) 3-kinases known to be a regulator of apoptosis. Methods: The cultured CNE3 epithelial tumor cells established from a poorly differentiated nasopharyngeal carcinoma were used in the present study. The expression of p85 was measured by Western Blotting. Apoptosis was assessed with fluorescence microscopy, DNA fragmentation assay, flow-cytometric analysis and caspase-3 cleavage. Results: Treatment of the CNE3 cells with 4HPR dose-dependently induced apoptosis as well as an elevation in the protein level of p85. The increased expression could be detected after 12 h of incubation with 4HPR at a concentration of 5 μM, and lasted for as long as 4HPR was present. A similar observation was made in another head and neck tumor derived cell line AC3. Inhibition of PI 3-kinases activity by the specific inhibitor LY294002 enhanced 4HPR-induced apoptosis, as detected by flow-cytometry and the increased cleavage of caspase-3. Conclusion: This study demonstrated that the expression of p85 was upregulated in response to 4HPR and suggests that the increased expression of p85 is likely to play a role other than in the activation of PI 3-kinases, which would protect the CNE3 cells against apoptosis.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/oraloncologyen_US
dc.relation.ispartofOral Oncologyen_US
dc.titleO-032. the relationship of p85 and the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)en_US
dc.typeArticleen_US
dc.identifier.emailWong, NS:nswong@hkucc.hku.hken_US
dc.identifier.authorityWong, NS=rp00340en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33747701567en_US
dc.identifier.hkuros56992-
dc.identifier.volume37en_US
dc.identifier.issueSUPPL. 1en_US
dc.identifier.spageS25en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridXia, Y=36986179900en_US
dc.identifier.scopusauthoridWong, NS=7202836641en_US
dc.identifier.scopusauthoridTideman, H=7005602469en_US

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