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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16269

    Title: DNA damage and endoplasmic reticulum stress mediated curcumin-induced cell cycle arrest and apoptosis in human lung carcinoma A-549 cells through the activation caspases cascade- and mitochondrial-dependent pathway
    Authors: 林松水;Lin, SS;黃宣榜;Huang, HP;楊家欣;Yang, JS;Wu, JY;夏德椿;Hsia, TC;林慶鐘;Lin, CC;Lin, CW;郭昭麟;Kuo, CL;Gibson Wood, W;鍾景光;Chung, Jing-Gung
    Contributors: 生物科技學系
    Date: 2008-06
    Issue Date: 2012-11-23 17:10:44 (UTC+8)
    Abstract: 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 μM in human lung cancer A-549 cells. In contrast, treatment with 5-10 μM 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 an 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 (ΔΨm), 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. © 2008 Elsevier Ireland Ltd. All rights reserved.
    Relation: CANCER LETTERS; 272(1):77-90.
    Appears in Collections:[生物科技學系] 期刊論文

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