期刊
CANCER LETTERS
卷 272, 期 1, 页码 77-90出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.06.031
关键词
Curcumin; Reactive oxygen species (ROS); Ca2+; Mitochondrial membrane potential (Delta Psi(m)); Caspase-3; Cell cycle arrest; Apoptosis
类别
资金
- National Science Council of Taiwan [NSC-94-2745-B-039-002-URD, NSC 95-2745-B-039-002-URD]
Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise Molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 mu M in human lung cancer A-549 cells. In contrast, treatment with 5-10 mu M of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) acting as ail indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca2+ levels and the mitochondrial membrane potential (Delta Psi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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