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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/8285

    Title: Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways
    Authors: Lin, Shuw-Yuan;林淑媛;Lai, Wan-Wen;賴婉文;Ho, Chin-Chin;何蓁蓁;Yu, Fu-Shun;游富順;Chen, Guang-Wei;陳光偉;Yang, Jai-Sing;楊家欣;Liu, Kuo-Ching;劉國慶;Lin, Meng-Liang;林孟亮;Wu, Ping-Ping;吳玢玢;Fan, Ming-Jen;范宗宸;Chung, Jing-Gung;鍾景光
    Contributors: Department of Biotechnology
    Keywords: ROS;ER stress;cell death;anthraquinone
    Date: 2009-01
    Issue Date: 2010-03-26 10:29:34 (UTC+8)
    Publisher: Asia University
    Abstract: Emodin was isolated from Rheum palmatum L. and exhibits an anticancer effect on human cancer cell lines, however, the molecular mechanisms of emodin-mediated apoptosis in human tongue cancer cells have not been fully investigated. In this study, treatment of human tongue cancer SCC-4 cells with various concentrations of emodin led to G(2)/M arrest through promoted p21 and Chk2 expression but inhibited cyclin B1 and cdc2; it also induced apoptosis through the pronounced release of cytochrome c from mitochondria and activations of caspase-9 and caspase-3. These events were accompanied by the generation of reactive oxygen species (ROS), disruption of mitochondrial membrane potential (Delta Psi(m)) and a decrease in the ratio of mitochondrial Bcl-2 and Box content; emodin also promoted the levels of GADD153 and GRP78. The free radical scavenger N-acetylcysteine and caspase inhibitors markedly blocked emodin-induced apoptosis. Taken together, these findings suggest that emodin mediated oxidative injury (DNA damage) based on ROS production and ER stress based on the levels of GADD153 and GRP78 that acts as an early and upstream change in the cell death cascade to caspase- and mitochondria-dependent signaling pathways, triggers mitochondrial dysfunction from Bcl-2 and Box modulation, mitochondrial cytochrome c release and caspase activation, consequently leading to apoptosis in SCC-4 cells.
    Relation: ANTICANCER RESEARCH,29 (1),327-335.
    Appears in Collections:[生物科技學系] 期刊論文

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