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KMID : 0620920110430040189
Experimental & Molecular Medicine
2011 Volume.43 No. 4 p.189 ~ p.196
Hydroxydibenzoylmethane induces apoptosis through repressing ornithine decarboxylase in human promyelocytic leukemia HL-60 cells
Wang Ming-Fu

Liao Ya-Fan
Hung Ying-Cheng
Lin Chih-Li
Hour Tzyh-Chyuan
Lue Ko-Huang
Hung Hui-Chih
Liu Guang-Yaw
Abstract
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.
KEYWORD
apoptosis, hydroxydibenzoylmethane, mitochondrial membrane potential, ornithine decarboxylase, reactive oxygen species
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