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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11703


    Title: Hydroxydibenzoylmethane induces apoptosis through repressing ornithine decarboxylase in human promyelocytic leukemia HL-60 cells.
    Authors: Wang, MF
    Liao, YF
    Hung, YC
    Lin, CL
    Hour, TC
    Lue, KH
    Hung, HC
    Liu, GY
    Keywords: apoptosis;hydroxydibenzoylmethane;mitochondrial membrane potential;ornithine decarboxylase;reactive oxygen species
    Date: 2011
    Issue Date: 2015-07-28T04:24:42Z (UTC)
    ISSN: 1226-3613
    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 (Δψ(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.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11703
    http://dx.doi.org/10.3858/emm.2011.43.4.023
    Relation: Exp Mol Med. 2011 Apr 30;43(4):189-96.
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