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Article: Involvement of both endoplasmic reticulum and mitochondria in photokilling of nasopharyngeal carcinoma cells by the photosensitizer Zn-BC-AM

TitleInvolvement of both endoplasmic reticulum and mitochondria in photokilling of nasopharyngeal carcinoma cells by the photosensitizer Zn-BC-AM
Authors
Issue Date2004
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
Citation
Biochemical Pharmacology, 2004, v. 68 n. 12, p. 2387-2396 How to Cite?
AbstractPhotodynamic therapy (PDT) is recently developed as an effective treatment for malignant disease. In PDT, the photosensitizer eradicates tumour by induction of apoptosis. In this study, we investigated the mechanistic actions of a recently developed second generation photosensitizer, Zn-BC-AM, on nasopharyngeal carcinoma (NPC) cells. Zn-BC-AM was found to localize in the mitochondria, endoplasmic reticulum (ER), and golgi body. Photoactivation of Zn-BC-AM loaded NPC cells resulted in a rapid collapse of mitochondrial membrane potential (Δψm) (15 min), followed by the release of cytochrome c (1 h), and activation of caspases-9 and -3 (4 h). Expression of ER chaperones Bip/Grp78 and Grp94, and ER resident lectin-like chaperone calnexin (CNX) was also enhanced in PDT-stressed NPC cells. Caspase-12, an important caspase involved in ER stress-induced apoptosis, was also activated. Inhibition of Ca2+ uptake into mitochondria by ruthenium red (RR) or loading the cells with EGTA-AM, an agent that buffers intracellular Ca2+ released from ER, resulted in a significant reduction of Zn-BC-AM PDT-induced cell death. These observations suggest that both ER and mitochondria are the subcellular targets of Zn-BC-AM. Effective activation of ER- and mitochondria-mediated apoptotic pathways is responsible for Zn-BC-AM PDT-induced NPC cell death. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/150859
ISSN
2015 Impact Factor: 5.091
2015 SCImago Journal Rankings: 2.263
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMak, NKen_US
dc.contributor.authorLi, KMen_US
dc.contributor.authorLeung, WNen_US
dc.contributor.authorWong, RNSen_US
dc.contributor.authorHuang, DPen_US
dc.contributor.authorLung, MLen_US
dc.contributor.authorLau, YKen_US
dc.contributor.authorChang, CKen_US
dc.date.accessioned2012-06-26T06:12:47Z-
dc.date.available2012-06-26T06:12:47Z-
dc.date.issued2004en_US
dc.identifier.citationBiochemical Pharmacology, 2004, v. 68 n. 12, p. 2387-2396en_US
dc.identifier.issn0006-2952en_US
dc.identifier.urihttp://hdl.handle.net/10722/150859-
dc.description.abstractPhotodynamic therapy (PDT) is recently developed as an effective treatment for malignant disease. In PDT, the photosensitizer eradicates tumour by induction of apoptosis. In this study, we investigated the mechanistic actions of a recently developed second generation photosensitizer, Zn-BC-AM, on nasopharyngeal carcinoma (NPC) cells. Zn-BC-AM was found to localize in the mitochondria, endoplasmic reticulum (ER), and golgi body. Photoactivation of Zn-BC-AM loaded NPC cells resulted in a rapid collapse of mitochondrial membrane potential (Δψm) (15 min), followed by the release of cytochrome c (1 h), and activation of caspases-9 and -3 (4 h). Expression of ER chaperones Bip/Grp78 and Grp94, and ER resident lectin-like chaperone calnexin (CNX) was also enhanced in PDT-stressed NPC cells. Caspase-12, an important caspase involved in ER stress-induced apoptosis, was also activated. Inhibition of Ca2+ uptake into mitochondria by ruthenium red (RR) or loading the cells with EGTA-AM, an agent that buffers intracellular Ca2+ released from ER, resulted in a significant reduction of Zn-BC-AM PDT-induced cell death. These observations suggest that both ER and mitochondria are the subcellular targets of Zn-BC-AM. Effective activation of ER- and mitochondria-mediated apoptotic pathways is responsible for Zn-BC-AM PDT-induced NPC cell death. © 2004 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharmen_US
dc.relation.ispartofBiochemical Pharmacologyen_US
dc.subject.meshAntineoplastic Agents - Chemical Synthesis - Pharmacologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshEndoplasmic Reticulum - Physiologyen_US
dc.subject.meshEnzyme Activation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshMetalloporphyrins - Chemical Synthesis - Pharmacologyen_US
dc.subject.meshMitochondria - Physiologyen_US
dc.subject.meshNasopharyngeal Neoplasms - Pathologyen_US
dc.subject.meshPhotochemotherapyen_US
dc.subject.meshPhotosensitizing Agents - Chemical Synthesis - Pharmacologyen_US
dc.subject.meshSubcellular Fractionsen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleInvolvement of both endoplasmic reticulum and mitochondria in photokilling of nasopharyngeal carcinoma cells by the photosensitizer Zn-BC-AMen_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.doi10.1016/j.bcp.2004.08.024en_US
dc.identifier.pmid15548385-
dc.identifier.scopuseid_2-s2.0-8844263679en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-8844263679&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume68en_US
dc.identifier.issue12en_US
dc.identifier.spage2387en_US
dc.identifier.epage2396en_US
dc.identifier.isiWOS:000225412400009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMak, NK=35582657000en_US
dc.identifier.scopusauthoridLi, KM=11439529600en_US
dc.identifier.scopusauthoridLeung, WN=7201504470en_US
dc.identifier.scopusauthoridWong, RNS=7402126957en_US
dc.identifier.scopusauthoridHuang, DP=7403891486en_US
dc.identifier.scopusauthoridLung, ML=7006411788en_US
dc.identifier.scopusauthoridLau, YK=7201403332en_US
dc.identifier.scopusauthoridChang, CK=7407039448en_US

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