Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/38162
標題: Curcumin induces apoptosis through an ornithine decarboxylase-dependent pathway in human promyelocytic leukemia HL-60 cells
作者: Liao, Y.F.
洪慧芝
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
期刊/報告no:: Life Sciences, Volume 82, Issue 7-8, Page(s) 367-375.
摘要: 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.
URI: http://hdl.handle.net/11455/38162
ISSN: 0024-3205
文章連結: http://dx.doi.org/10.1016/j.lfs.2007.11.022
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