Journal
ANATOMICAL SCIENCE INTERNATIONAL
Volume 83, Issue 4, Pages 261-266Publisher
SPRINGER
DOI: 10.1111/j.1447-073X.2008.00241.x
Keywords
blue native PAGE; furanonaphthoquinone; menadione; reactive oxygen species; voltage-dependent anion channel 1
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Funding
- Japan Society for the Promotion of Science [15591664, 17591899]
- Kanazawa Medical University [S2003-12, S2004-12, S2007-9, C2007-4]
- Grants-in-Aid for Scientific Research [15591664, 17591899] Funding Source: KAKEN
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The authors recently demonstrated that the mitochondrial voltage-dependent anion channel 1 (VDAC1) is involved in the sensitivity of cancer cells to furanonaphthoquinone (FNQ). The aim of the present study was to investigate whether mitochondrial VDAC1 reduces quinone antitumor drugs. The VDAC1 purified by immunoprecipitation reduced FNQ in the presence of nicotinamide adenine dinucleotide (NADH) and produced H2O2. Blue native polyacrylamide gel electrophoresis demonstrated that the band that reduced FNQ NADH-dependently mainly included VDAC1. Because H2O2 generation in catalyzing FNQ with NADH caused mitochondrial damage, the cytotoxic activity of FNQ was induced by VDAC1. In the quinone antitumor drugs, menadione (VK3), adriamycin and mitomycin C, mitochondrial VDAC1 bioreductively activated VK3. These results demonstrate that mitochondrial VDAC1 is a pharmacologic target for the treatment of tumor.
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