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Conference Paper: Gold porphyrin (III) 1a induced apoptosis by caspase dependent and independent mitochondrial death pathways dependent of reactive oxygen species

TitleGold porphyrin (III) 1a induced apoptosis by caspase dependent and independent mitochondrial death pathways dependent of reactive oxygen species
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research
Citation
The 96th Annual Meeting of AACR, Anaheim, CA, 16-20 April 2005. In Cancer Research, 2005, v. 65 n. 9s, p. 407 Abstract no. 1729 How to Cite?
AbstractThe application of gold (III) complexes as potential antitumor drug lead with higher cytotoxicity and fewer side effects than existing metal antitumor drugs has been actively pursued in recent years. Our previous findings (Che CM et al, Chem. Commun., 14, 1718-1719, and recent data) showed that the gold (III) meso-tetraarylporphyrin 1a induced apoptosis by initiating a series of complex reactions that caused unbalance between pro-apoptotic and anti-apoptotic signals in human carcinoma cell lines. The mechanism of cancer cell apoptosis induced by gold (III) porphyrin 1a was investigated in the current study. Human nasopharyngeal carcinoma cell line (HONE1) exposed to gold (III) porphyrin 1a underwent apoptosis after 24 h, with formation of DNA ladder and cleavage of PARP-1. Proteomic studies revealed the alteration of several cellular protein expressions in cancer cells after treatment with the drug. These proteins include enzymes participated in energy production and proteins involved in cellular redox balance, suggesting that mitochondrion maybe the main target of gold (III) porphyrin 1a. There was a quick attenuation of mitochondrial membrane potential (ΔΨm) with the release of cytochrome c and apoptosis inducing factor (AIF) following gold (III) porphyrin 1a treatment. Cytochrome c in turn activated caspase 9 and caspase 3. Co-treatment with caspase inhibitor (z-VAD.fmk) revealed that the activated caspases acting in conjunction with apoptosis inducing factor initiated the apoptosis pathways. Further study showed that reactive oxygen species was involved in gold (III) porphyrin 1a induced apoptosis. Pretreatment with NAC or BSO altered the process of apoptosis, indicating that oxidative stress was associated with cytotoxicity of gold (III) porphyrin 1a. Taken together of these findings, gold (III) porphyrin 1a induces apoptosis through both caspase-dependent and -independent mitochondrial pathways that initiated by oxidative stress.
Persistent Identifierhttp://hdl.handle.net/10722/96979
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorHe, Qen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorChiu, Jen_HK
dc.date.accessioned2010-09-25T16:52:01Z-
dc.date.available2010-09-25T16:52:01Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 96th Annual Meeting of AACR, Anaheim, CA, 16-20 April 2005. In Cancer Research, 2005, v. 65 n. 9s, p. 407 Abstract no. 1729-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/96979-
dc.description.abstractThe application of gold (III) complexes as potential antitumor drug lead with higher cytotoxicity and fewer side effects than existing metal antitumor drugs has been actively pursued in recent years. Our previous findings (Che CM et al, Chem. Commun., 14, 1718-1719, and recent data) showed that the gold (III) meso-tetraarylporphyrin 1a induced apoptosis by initiating a series of complex reactions that caused unbalance between pro-apoptotic and anti-apoptotic signals in human carcinoma cell lines. The mechanism of cancer cell apoptosis induced by gold (III) porphyrin 1a was investigated in the current study. Human nasopharyngeal carcinoma cell line (HONE1) exposed to gold (III) porphyrin 1a underwent apoptosis after 24 h, with formation of DNA ladder and cleavage of PARP-1. Proteomic studies revealed the alteration of several cellular protein expressions in cancer cells after treatment with the drug. These proteins include enzymes participated in energy production and proteins involved in cellular redox balance, suggesting that mitochondrion maybe the main target of gold (III) porphyrin 1a. There was a quick attenuation of mitochondrial membrane potential (ΔΨm) with the release of cytochrome c and apoptosis inducing factor (AIF) following gold (III) porphyrin 1a treatment. Cytochrome c in turn activated caspase 9 and caspase 3. Co-treatment with caspase inhibitor (z-VAD.fmk) revealed that the activated caspases acting in conjunction with apoptosis inducing factor initiated the apoptosis pathways. Further study showed that reactive oxygen species was involved in gold (III) porphyrin 1a induced apoptosis. Pretreatment with NAC or BSO altered the process of apoptosis, indicating that oxidative stress was associated with cytotoxicity of gold (III) porphyrin 1a. Taken together of these findings, gold (III) porphyrin 1a induces apoptosis through both caspase-dependent and -independent mitochondrial pathways that initiated by oxidative stress.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleGold porphyrin (III) 1a induced apoptosis by caspase dependent and independent mitochondrial death pathways dependent of reactive oxygen speciesen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWang, Y: ywang3@hkucc.hku.hken_HK
dc.identifier.emailHe, Q: qyhe@hkucc.hku.hken_HK
dc.identifier.emailChe, CM: cmche@hku.hken_HK
dc.identifier.emailChiu, J: jfchiu@hkucc.hku.hken_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.identifier.hkuros106714en_HK

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