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Article: Role of p38 MAPKs in hypericin photodynamic therapy-induced apoptosis of nasopharyngeal carcinoma cells

TitleRole of p38 MAPKs in hypericin photodynamic therapy-induced apoptosis of nasopharyngeal carcinoma cells
Authors
Issue Date2009
PublisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/118493575/home
Citation
Photochemistry And Photobiology, 2009, v. 85 n. 5, p. 1207-1217 How to Cite?
AbstractThe present study aims to determine the role of mitogen-activated protein kinases (MAPKs) in hypericin-mediated photodynamic therapy (HY-PDT)-induced apoptosis of the HK-1 nasopharyngeal carcinoma (NPC) cells. HY-PDT was found to induce proteolytic cleavage of procaspase-9 and -3 in HK-1 cells. Apoptotic nuclei were observed at 6 h after PDT whereas B-cell leukemia/lymphoma-2- associated-X-protein (Bax) translocation and formation of Bax channel is responsible for the cell death. Increase in phosphorylation of p38 MAPKs and c-Jun N-terminal kinase 1/2 (JNK1/2) was detected at 15-30 min after HY-PDT. The appearance of phosphorylated form of p38 MAPKs and JNK1/2 was inhibited by the singlet oxygen scavenger l-histidine. HY-PDT-induced cell death was enhanced by the chemical inhibitors for p38 MAPKs (SB202190 and SB203580), but not by the JNKs inhibitor SP600125. Knockdown of the p38α and p38β MAPK isoforms by small interfering RNA (siRNA) are more effective than the p38 in enhancing PDT-induced cell death. Augmentation of apoptosis by p38α or p38β knockdown is also correlated with the increased proteolytic cleavage of procaspase-9 after HY-PDT treatment. Our results suggested that HY-PDT activated p38 MAPKs through the production of singlet oxygen. Inhibition of p38 MAPKs with chemical inhibitors or siRNA enhances HY-PDT-induced apoptosis of the HK-1 NPC cells. © 2009 The American Society of Photobiology.
Persistent Identifierhttp://hdl.handle.net/10722/150828
ISSN
2015 Impact Factor: 2.008
2015 SCImago Journal Rankings: 0.630
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong KongHKBU 2458/06M
Funding Information:

This work was supported by the Research Grants Council of Hong Kong (project HKBU 2458/06M).

References

 

DC FieldValueLanguage
dc.contributor.authorChan, PSen_US
dc.contributor.authorKoon, HKen_US
dc.contributor.authorWu, ZGen_US
dc.contributor.authorWong, RNSen_US
dc.contributor.authorLung, MLen_US
dc.contributor.authorChang, CKen_US
dc.contributor.authorMak, NKen_US
dc.date.accessioned2012-06-26T06:11:37Z-
dc.date.available2012-06-26T06:11:37Z-
dc.date.issued2009en_US
dc.identifier.citationPhotochemistry And Photobiology, 2009, v. 85 n. 5, p. 1207-1217en_US
dc.identifier.issn0031-8655en_US
dc.identifier.urihttp://hdl.handle.net/10722/150828-
dc.description.abstractThe present study aims to determine the role of mitogen-activated protein kinases (MAPKs) in hypericin-mediated photodynamic therapy (HY-PDT)-induced apoptosis of the HK-1 nasopharyngeal carcinoma (NPC) cells. HY-PDT was found to induce proteolytic cleavage of procaspase-9 and -3 in HK-1 cells. Apoptotic nuclei were observed at 6 h after PDT whereas B-cell leukemia/lymphoma-2- associated-X-protein (Bax) translocation and formation of Bax channel is responsible for the cell death. Increase in phosphorylation of p38 MAPKs and c-Jun N-terminal kinase 1/2 (JNK1/2) was detected at 15-30 min after HY-PDT. The appearance of phosphorylated form of p38 MAPKs and JNK1/2 was inhibited by the singlet oxygen scavenger l-histidine. HY-PDT-induced cell death was enhanced by the chemical inhibitors for p38 MAPKs (SB202190 and SB203580), but not by the JNKs inhibitor SP600125. Knockdown of the p38α and p38β MAPK isoforms by small interfering RNA (siRNA) are more effective than the p38 in enhancing PDT-induced cell death. Augmentation of apoptosis by p38α or p38β knockdown is also correlated with the increased proteolytic cleavage of procaspase-9 after HY-PDT treatment. Our results suggested that HY-PDT activated p38 MAPKs through the production of singlet oxygen. Inhibition of p38 MAPKs with chemical inhibitors or siRNA enhances HY-PDT-induced apoptosis of the HK-1 NPC cells. © 2009 The American Society of Photobiology.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/118493575/homeen_US
dc.relation.ispartofPhotochemistry and Photobiologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshHumansen_US
dc.subject.meshNasopharyngeal Neoplasms - Drug Therapy - Pathologyen_US
dc.subject.meshPerylene - Analogs & Derivatives - Pharmacology - Therapeutic Useen_US
dc.subject.meshPhotochemotherapyen_US
dc.subject.meshRna, Small Interferingen_US
dc.subject.meshP38 Mitogen-Activated Protein Kinases - Metabolismen_US
dc.titleRole of p38 MAPKs in hypericin photodynamic therapy-induced apoptosis of nasopharyngeal carcinoma cellsen_US
dc.typeArticleen_US
dc.identifier.emailLung, ML:mlilung@hku.hken_US
dc.identifier.authorityLung, ML=rp00300en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1751-1097.2009.00572.xen_US
dc.identifier.pmid19496992-
dc.identifier.scopuseid_2-s2.0-69649097192en_US
dc.identifier.hkuros162656-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-69649097192&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume85en_US
dc.identifier.issue5en_US
dc.identifier.spage1207en_US
dc.identifier.epage1217en_US
dc.identifier.isiWOS:000269463700021-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChan, PS=35075787200en_US
dc.identifier.scopusauthoridKoon, HK=12766487800en_US
dc.identifier.scopusauthoridWu, ZG=8218909600en_US
dc.identifier.scopusauthoridWong, RNS=35270797800en_US
dc.identifier.scopusauthoridLung, ML=7006411788en_US
dc.identifier.scopusauthoridChang, CK=35242004200en_US
dc.identifier.scopusauthoridMak, NK=35582657000en_US

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