Journal
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume 43, Issue 4, Pages 189-196Publisher
NATURE PUBLISHING GROUP
DOI: 10.3858/emm.2011.43.4.023
Keywords
apoptosis; hydroxydibenzoylmethane; mitochondrial membrane potential; ornithine decarboxylase; reactive oxygen species
Funding
- Chung Shan Medical University
- Tung's Taichung MetroHarbor hospital [CSMU-TTM-098-005]
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Ornithine decarboxylase (ODC) is the rate-limiting enzyme in polyamine biosynthesis and a target for chemoprevention. Hydroxydibenzoylmethane (HDB), a derivative of dibenzoylmethane of licorice, is a promising chemopreventive agent. In this paper, we investigated whether HDB would inhibit the ODC pathway to enhance apoptosis in human promyelocytic leukemia HL-60 cells. We found ODC enzyme activity was reduced during HDB treatment. Overexpression of ODC in HL-60 parental cells could reduce HDB-induced apoptosis, which leads to loss of mitochondrial membrane potential (Delta psi(m)), through lessening intracellular ROS. Furthermore, ODC overexpression protected cytochrome c release and the activation of caspase-3 following HDB treatment. The results demonstrated HDB-induced apoptosis was through a mechanism of down-regulation of ODC and occurred along a ROS-dependent mitochondria-mediated pathway.
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