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標題: Curcumin induces apoptosis through an ornithine decarboxylase-dependent pathway in human promyelocytic leukemia HL-60 cells
作者: Liao, Y.F.
Hung, H.C.
Hour, T.C.
Hsu, P.C.
Kao, M.C.
Tsay, G.J.
Liu, G.Y.
關鍵字: curcumin;apoptosis;ornithine decarboxylase;reactive oxygen species;factor-kappa-b;methotrexate-induced apoptosis;oxygen species;production;regulated gene-products;human breast-cancer;alpha-difluoromethylornithine;cytochrome-c;mouse skin;pkc-delta;in-vitro
Project: Life Sciences
期刊/報告no:: Life Sciences, Volume 82, Issue 7-8, Page(s) 367-375.
Curcumin, a well-known dietary pigment derived from the food flavoring turmeric (Curcuma longa) exhibits anti-proliferative, anti-inflammatory, and anti-oxidative activities. Recently, studies have shown that a chemopreventive effect of curcumin could be due to the hyperproduction of reactive oxygen species (ROS) inducing apoptosis in tumor cells. In our previous studies, ornithine decarboxylase (ODC) overexpression prevented tumor necrosis factor alpha (TNF-alpha)- and methotrexate-induced apoptosis via reduction of ROS. Furthermore, ODC is the rate-limiting enzyme in polyamine biosynthesis and a target for chemoprevention. In this study, we found that enzyme activity and protein expression of ODC were reduced during curcumin treatment. Overexpression of ODC in human promyelocytic leukemia HL-60 parental cells could reduce curcumin-induced apoptosis, which leads to loss of mitochondrial membrane potential (Delta psi(m)), through reducing intracellular ROS. Moreover, ODC overexpression prevented cytochrome c release and the activation of caspase-9 and caspase-3 following curcumin treatment. These results demonstrate that curcumin-induced apoptosis occurs through a mechanism of down-regulating ODC and along a ROS-dependent mitochondria-mediated pathway. (C) 2007 Elsevier Inc. All rights reserved.
ISSN: 0024-3205
DOI: 10.1016/j.lfs.2007.11.022
Appears in Collections:生命科學系所

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