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Gold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species
Wang Y.1; He Q.-Y.1; Sun R.W.-Y.1; Che C.-M.1; Chiu J.-F.1
2005-12-15
Source PublicationCancer Research
ISSN00085472
Volume65Issue:24Pages:11553-11564
Abstract

Apoptosis 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 (ΔΨ) 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 ΔΨ. 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.

DOI10.1158/0008-5472.CAN-05-2867
URLView the original
Indexed BySCI
Language英语
WOS Research AreaOncology
WOS SubjectOncology
WOS IDWOS:000234159100042
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被引频次[WOS]:144   [WOS记录]     [WOS相关记录]
Document TypeJournal article
专题Institute of Chinese Medical Sciences
Corresponding AuthorChe C.-M.
Affiliation1.Institute of Molecular Technology for Drug Discovery and Synthesis, Hong Kong
2.The University of Hong Kong
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GB/T 7714
Wang Y.,He Q.-Y.,Sun R.W.-Y.,et al. Gold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species[J]. Cancer Research,2005,65(24):11553-11564.
APA Wang Y.,He Q.-Y.,Sun R.W.-Y.,Che C.-M.,&Chiu J.-F..(2005).Gold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species.Cancer Research,65(24),11553-11564.
MLA Wang Y.,et al."Gold(III) porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species".Cancer Research 65.24(2005):11553-11564.
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