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Article: Gold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species

TitleGold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2005, v. 65 n. 24, p. 11553-11564 How to Cite?
AbstractApoptosis is a tightly controlled multistep mechanism of cell death, and mitochondria are considered to play a central role in this process. Mitochondria initiate two distinct apoptosis pathways, one caspase-dependent and the other caspase-independent. In addition, mitochondrial production of reactive oxygen species (ROS) seems to play a role in cell death. Most chemotherapeutic agents induce apoptosis through at least one of these pathways. The post-initiation mechanisms of gold(III) porphyrin la were investigated in this study. HONE1 cells exposed to gold(III) porphyrin la underwent apoptosis after 24 hours. Functional proteomic studies revealed the alteration of several cytoplasmic protein expressions in HONE1 cells after treatment with the drug. These proteins include enzymes participating in energy production and proteins involved in cellular redox balance. There was a quick attenuation of mitochondrial membrane potential (ΔΨm) with the alterations of Bcl-2 family proteins, the release of cytochrome c, and apoptosis-inducing factor (AIF) following gold(III) porphyrin la treatment. Cytochrome c in turn activated caspase-9 and caspase-3. Cotreatment with caspase inhibitor (zVAD-fmk) showed that the activated caspases worked in conjunction with AIF-initiated apoptosis pathways. Further study showed that ROS played a part in gold(III) porphyrin 1a-induced apoptosis by regulating ΔΨm. In summary, gold(III) porphyrin la induced apoptosis through both caspase-dependent and caspase-independent mitochondrial pathways, and intracellular oxidation affected gold(III) porphyrin 1a-induced apoptosis. These results support a role for gold(III) porphyrin la as a promising anticancer drug lead and as a possible novel therapeutic agent directed toward the mitochondria. ©2005 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/69785
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorHe, QYen_HK
dc.contributor.authorSun, RWYen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorChiu, JFen_HK
dc.date.accessioned2010-09-06T06:16:49Z-
dc.date.available2010-09-06T06:16:49Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Research, 2005, v. 65 n. 24, p. 11553-11564en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/69785-
dc.description.abstractApoptosis is a tightly controlled multistep mechanism of cell death, and mitochondria are considered to play a central role in this process. Mitochondria initiate two distinct apoptosis pathways, one caspase-dependent and the other caspase-independent. In addition, mitochondrial production of reactive oxygen species (ROS) seems to play a role in cell death. Most chemotherapeutic agents induce apoptosis through at least one of these pathways. The post-initiation mechanisms of gold(III) porphyrin la were investigated in this study. HONE1 cells exposed to gold(III) porphyrin la underwent apoptosis after 24 hours. Functional proteomic studies revealed the alteration of several cytoplasmic protein expressions in HONE1 cells after treatment with the drug. These proteins include enzymes participating in energy production and proteins involved in cellular redox balance. There was a quick attenuation of mitochondrial membrane potential (ΔΨm) with the alterations of Bcl-2 family proteins, the release of cytochrome c, and apoptosis-inducing factor (AIF) following gold(III) porphyrin la treatment. Cytochrome c in turn activated caspase-9 and caspase-3. Cotreatment with caspase inhibitor (zVAD-fmk) showed that the activated caspases worked in conjunction with AIF-initiated apoptosis pathways. Further study showed that ROS played a part in gold(III) porphyrin 1a-induced apoptosis by regulating ΔΨm. In summary, gold(III) porphyrin la induced apoptosis through both caspase-dependent and caspase-independent mitochondrial pathways, and intracellular oxidation affected gold(III) porphyrin 1a-induced apoptosis. These results support a role for gold(III) porphyrin la as a promising anticancer drug lead and as a possible novel therapeutic agent directed toward the mitochondria. ©2005 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.titleGold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen speciesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=65&spage=11553&epage=11564&date=2005&atitle=Gold(III)+porphyrin+1a+induced+apoptosis+by+mitochondrial+death+pathways+related+to+reactive+oxygen+species+en_HK
dc.identifier.emailSun, RWY:rwysun@hku.hken_HK
dc.identifier.emailChe, CM:cmche@hku.hken_HK
dc.identifier.authoritySun, RWY=rp00781en_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-05-2867en_HK
dc.identifier.pmid16357165-
dc.identifier.scopuseid_2-s2.0-29244451873en_HK
dc.identifier.hkuros118002en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29244451873&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume65en_HK
dc.identifier.issue24en_HK
dc.identifier.spage11553en_HK
dc.identifier.epage11564en_HK
dc.identifier.isiWOS:000234159100042-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=7601510411en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK
dc.identifier.scopusauthoridSun, RWY=26325835800en_HK
dc.identifier.scopusauthoridChe, CM=7102442791en_HK
dc.identifier.scopusauthoridChiu, JF=7201501692en_HK

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