File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Modulation of gold(III) porphyrin 1a-induced apoptosis by mitogen-activated protein kinase signaling pathways

TitleModulation of gold(III) porphyrin 1a-induced apoptosis by mitogen-activated protein kinase signaling pathways
Authors
KeywordsApoptosis
Gold(III) compound
MAPK
Mitochondria
Proteomics
Tyrosine phosphorylation
Issue Date2008
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
Citation
Biochemical Pharmacology, 2008, v. 75 n. 6, p. 1282-1291 How to Cite?
AbstractGold(III) porphyrin 1a is a novel gold(III) complex with selective anticancer effect in a number of human carcinoma cell lines. We have previously shown that gold(III) porphyrin 1a mediated mitochondrial transmembrane potential (ΔΨm) depletion, leading to cytochrome c release, nucleus translocation of apoptosis-inducing factor (AIF), and generation of reactive oxygen species (ROS). The current study addressed gold(III) porphyrin 1a-induced phosphoproteome alterations and modulation of cell death by the mitogen-activated protein kinase (MAPK) family proteins. ERK and p38MAPK were transiently activated upon gold(III) porphyrin 1a treatment. Inhibition of p38MAPK phosphorylation rescued gold(III) porphyrin 1a-induced cell death upstream of caspase activation. Attenuation of ΔΨm was the primary effect of gold(III) porphyrin 1a leading to p38MAPK phosphorylation. Further functional proteomic study suggested that differential regulation of phosphotyrosine proteins were related to p38MAPK activation in gold(III) porphyrin 1a-induced signal transduction cascade. In summary, p38MAPK modulated gold(III) porphyrin 1a-induced cell death downstream of mitochondria, and phosphorylation of multiple proteins also involved in this process. These results suggested that gold(III) porphyrin 1a is a promising anticancer agent directed toward the mitochondria. © 2007 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67400
ISSN
2015 Impact Factor: 5.091
2015 SCImago Journal Rankings: 2.263
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorHe, QYen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorSun, RWYen_HK
dc.contributor.authorChiu, JFen_HK
dc.date.accessioned2010-09-06T05:54:49Z-
dc.date.available2010-09-06T05:54:49Z-
dc.date.issued2008en_HK
dc.identifier.citationBiochemical Pharmacology, 2008, v. 75 n. 6, p. 1282-1291en_HK
dc.identifier.issn0006-2952en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67400-
dc.description.abstractGold(III) porphyrin 1a is a novel gold(III) complex with selective anticancer effect in a number of human carcinoma cell lines. We have previously shown that gold(III) porphyrin 1a mediated mitochondrial transmembrane potential (ΔΨm) depletion, leading to cytochrome c release, nucleus translocation of apoptosis-inducing factor (AIF), and generation of reactive oxygen species (ROS). The current study addressed gold(III) porphyrin 1a-induced phosphoproteome alterations and modulation of cell death by the mitogen-activated protein kinase (MAPK) family proteins. ERK and p38MAPK were transiently activated upon gold(III) porphyrin 1a treatment. Inhibition of p38MAPK phosphorylation rescued gold(III) porphyrin 1a-induced cell death upstream of caspase activation. Attenuation of ΔΨm was the primary effect of gold(III) porphyrin 1a leading to p38MAPK phosphorylation. Further functional proteomic study suggested that differential regulation of phosphotyrosine proteins were related to p38MAPK activation in gold(III) porphyrin 1a-induced signal transduction cascade. In summary, p38MAPK modulated gold(III) porphyrin 1a-induced cell death downstream of mitochondria, and phosphorylation of multiple proteins also involved in this process. These results suggested that gold(III) porphyrin 1a is a promising anticancer agent directed toward the mitochondria. © 2007 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharmen_HK
dc.relation.ispartofBiochemical Pharmacologyen_HK
dc.rightsBiochemical Pharmacology. Copyright © Elsevier Inc.en_HK
dc.subjectApoptosisen_HK
dc.subjectGold(III) compounden_HK
dc.subjectMAPKen_HK
dc.subjectMitochondriaen_HK
dc.subjectProteomicsen_HK
dc.subjectTyrosine phosphorylationen_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCaspase 3 - metabolismen_HK
dc.subject.meshCaspase 9 - metabolismen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMAP Kinase Signaling System - drug effectsen_HK
dc.subject.meshMembrane Potential, Mitochondrial - drug effectsen_HK
dc.subject.meshMetalloporphyrins - pharmacologyen_HK
dc.subject.meshPhosphoproteins - metabolismen_HK
dc.subject.meshPhosphorylationen_HK
dc.subject.meshPhosphotyrosine - metabolismen_HK
dc.subject.meshReactive Oxygen Species - metabolismen_HK
dc.subject.meshp38 Mitogen-Activated Protein Kinases - metabolismen_HK
dc.titleModulation of gold(III) porphyrin 1a-induced apoptosis by mitogen-activated protein kinase signaling pathwaysen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-2952&volume=75&spage=1282&epage=1291&date=2008&atitle=Modulation+of+gold(III)+porphyrin+1a-induced+apoptosis+by+mitogen-activated+protein+kinase+signaling+pathwaysen_HK
dc.identifier.emailChe, CM:cmche@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailSun, RWY:rwysun@hku.hken_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authoritySun, RWY=rp00781en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bcp.2007.11.024en_HK
dc.identifier.pmid18241839-
dc.identifier.scopuseid_2-s2.0-39749155663en_HK
dc.identifier.hkuros141593en_HK
dc.identifier.volume75en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1282en_HK
dc.identifier.epage1291en_HK
dc.identifier.isiWOS:000254687800004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=35075333300en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK
dc.identifier.scopusauthoridChe, CM=7102442791en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridSun, RWY=26325835800en_HK
dc.identifier.scopusauthoridChiu, JF=7201501692en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats