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Article: Targeted inhibition of the EGFR pathways enhances Zn-BC-AM PDT-induced apoptosis in well-differentiated nasopharyngeal carcinoma cells

TitleTargeted inhibition of the EGFR pathways enhances Zn-BC-AM PDT-induced apoptosis in well-differentiated nasopharyngeal carcinoma cells
Authors
KeywordsEGFR
NPC
Photodynamic therapy
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
Citation
Journal Of Cellular Biochemistry, 2009, v. 108 n. 6, p. 1356-1363 How to Cite?
AbstractEpidermal growth factor receptor (EGFR), a receptor often expressed in nasopharyngeal carcinoma (NPC) cells, is one of the recently identified molecular targets in cancer treatment. In the present study, the effects of combined treatment of Zn-BC-AM PDT with an EGFR inhibitor AG1478 were investigated. Well-differentiated NPC HK-1 cells were subjected to PDT with 1 μM of Zn-BC-AM and were irradiated at a light dose of 1 J/cm2 in the presence or absence of EGFR inhibitor AG1478. Specific protein kinase inhibitors of downstream EGFR targets were also used in the investigation. EGFR, Akt, and ERK were found constitutively activated in HK-1 cells and the activities could be inhibited by the EGFR inhibitor AG1478. A sub-lethal concentration of AG1478 was found to further enhance the irreversible cell damage induced by Zn-BC-AM PDT in HK-1 cells. Pre-incubation of the cells with specific inhibitors of EGFR (AG1478), PI3k/Akt (LY294002), or MEK/ERK (PD98059) before light irradiation were found to enhance Zn-BC-AM PDT-induced formation of apoptotic cells. The efficacy of Zn-BC-AM PDT can be increased through the inhibition of EGFR/PI3K/Akt and EGFR/MEK/ERK signaling pathways in NPC cells. Combination therapy with Zn-BC-AM PDT and EGFR inhibitors may further be developed for the treatment of advanced NPC. © 2009 Wiley-Liss, Inc.
Persistent Identifierhttp://hub.hku.hk/handle/10722/128964
ISSN
2015 Impact Factor: 3.446
2015 SCImago Journal Rankings: 1.520
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKBU 2458/06M
Faculty DepartmentFRG/07-08/1-57
Funding Information:

This work was supported by the Research Grants Council of Hong Kong (project no. HKBU 2458/06M) and the Faculty Department Grant (No. FRG/07-08/1-57).

References

 

DC FieldValueLanguage
dc.contributor.authorKoon, HKen_HK
dc.contributor.authorChan, PSen_HK
dc.contributor.authorWong, RNSen_HK
dc.contributor.authorWu, ZGen_HK
dc.contributor.authorLung, MLen_HK
dc.contributor.authorChang, CKen_HK
dc.contributor.authorMak, NKen_HK
dc.date.accessioned2010-11-29T07:15:05Z-
dc.date.available2010-11-29T07:15:05Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Cellular Biochemistry, 2009, v. 108 n. 6, p. 1356-1363en_HK
dc.identifier.issn0730-2312en_HK
dc.identifier.urihttp://hub.hku.hk/handle/10722/128964-
dc.description.abstractEpidermal growth factor receptor (EGFR), a receptor often expressed in nasopharyngeal carcinoma (NPC) cells, is one of the recently identified molecular targets in cancer treatment. In the present study, the effects of combined treatment of Zn-BC-AM PDT with an EGFR inhibitor AG1478 were investigated. Well-differentiated NPC HK-1 cells were subjected to PDT with 1 μM of Zn-BC-AM and were irradiated at a light dose of 1 J/cm2 in the presence or absence of EGFR inhibitor AG1478. Specific protein kinase inhibitors of downstream EGFR targets were also used in the investigation. EGFR, Akt, and ERK were found constitutively activated in HK-1 cells and the activities could be inhibited by the EGFR inhibitor AG1478. A sub-lethal concentration of AG1478 was found to further enhance the irreversible cell damage induced by Zn-BC-AM PDT in HK-1 cells. Pre-incubation of the cells with specific inhibitors of EGFR (AG1478), PI3k/Akt (LY294002), or MEK/ERK (PD98059) before light irradiation were found to enhance Zn-BC-AM PDT-induced formation of apoptotic cells. The efficacy of Zn-BC-AM PDT can be increased through the inhibition of EGFR/PI3K/Akt and EGFR/MEK/ERK signaling pathways in NPC cells. Combination therapy with Zn-BC-AM PDT and EGFR inhibitors may further be developed for the treatment of advanced NPC. © 2009 Wiley-Liss, Inc.en_HK
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503en_HK
dc.relation.ispartofJournal of Cellular Biochemistryen_HK
dc.rightsThe definitive version is available at www3.interscience.wiley.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectEGFRen_HK
dc.subjectNPCen_HK
dc.subjectPhotodynamic therapyen_HK
dc.subject.meshAntineoplastic Agents - therapeutic use-
dc.subject.meshMetalloporphyrins - therapeutic use-
dc.subject.meshNasopharyngeal Neoplasms - drug therapy - metabolism-
dc.subject.meshPhotochemotherapy-
dc.subject.meshPhotosensitizing Agents - therapeutic use-
dc.titleTargeted inhibition of the EGFR pathways enhances Zn-BC-AM PDT-induced apoptosis in well-differentiated nasopharyngeal carcinoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0730-2312&volume=108&issue=6&spage=1356&epage=1363&date=2009&atitle=Targeted+inhibition+of+the+EGFR+pathways+enhances+Zn-BC-AM+PDT-induced+apoptosis+in+well-differentiated+nasopharyngeal+carcinoma+cells-
dc.identifier.emailLung, ML:mlilung@hku.hken_HK
dc.identifier.authorityLung, ML=rp00300en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1002/jcb.22366en_HK
dc.identifier.pmid19816982-
dc.identifier.scopuseid_2-s2.0-71749101304en_HK
dc.identifier.hkuros174420-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-71749101304&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume108en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1356en_HK
dc.identifier.epage1363en_HK
dc.identifier.isiWOS:000272649900013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKoon, HK=12766487800en_HK
dc.identifier.scopusauthoridChan, PS=35075787200en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK
dc.identifier.scopusauthoridWu, ZG=35076845600en_HK
dc.identifier.scopusauthoridLung, ML=7006411788en_HK
dc.identifier.scopusauthoridChang, CK=7407039448en_HK
dc.identifier.scopusauthoridMak, NK=35582657000en_HK

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