KMID : 0620920110430040189
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Experimental & Molecular Medicine 2011 Volume.43 No. 4 p.189 ~ p.196
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Hydroxydibenzoylmethane induces apoptosis through repressing ornithine decarboxylase in human promyelocytic leukemia HL-60 cells
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Wang Ming-Fu
Liao Ya-Fan Hung Ying-Cheng Lin Chih-Li Hour Tzyh-Chyuan Lue Ko-Huang Hung Hui-Chih Liu Guang-Yaw
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Abstract
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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 (¥Ä¥÷ 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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KEYWORD
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apoptosis, hydroxydibenzoylmethane, mitochondrial membrane potential, ornithine decarboxylase, reactive oxygen species
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