Curcumin induces apoptosis through an ornithine decarboxylase-dependent pathway in human promyelocytic leukemia HL-60 cells.

doi:10.1016/j.lfs.2007.11.022

中山醫學大學機構典藏 CSMUIR > 醫學院 > 免疫學研究所 > 期刊論文 > Item 310902500/11715

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题名:	Curcumin induces apoptosis through an ornithine decarboxylase-dependent pathway in human promyelocytic leukemia HL-60 cells.
作者:	Liao, YF Hung, HC Hour, TC Hsu, PC Kao, MC Tsay, GJ Liu, GY
贡献者:	中山醫學大學
关键词:	Curcumin;Apoptosis;Ornithine decarboxylase;Reactive oxygen species
日期:	2008
上传时间:	2015-07-28T05:39:40Z (UTC)
ISSN:	0024-3205
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 (Deltapsi(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.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11715 http://dx.doi.org/10.1016/j.lfs.2007.11.022
關聯:	Life Sci. 2008 Feb 13;82(7-8):367-75.
显示于类别:	[免疫學研究所] 期刊論文

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