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    题名: Emodin Induces Apoptosis of Human Tongue Squamous Cancer SCC-4 Cells through Reactive Oxygen Species and Mitochondria-dependent Pathways
    作者: 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
    贡献者: Department of Biotechnology
    关键词: ROS;ER stress;cell death;anthraquinone
    日期: 2009-01
    上传时间: 2010-03-26 10:29:34 (UTC+8)
    出版者: Asia University
    摘要: 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.
    關聯: ANTICANCER RESEARCH,29 (1),327-335.
    显示于类别:[生物科技學系] 期刊論文

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