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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16505

    Title: Cantharidin induces apoptosis in human bladder cancer TSGH 8301 cells through mitochondria-dependent signal pathways
    Authors: ;KUO, JEHN-HWA;朱永麟;CHU, YUNG-LIN;楊家欣;YANG, JAI-SING;林景彬;LIN, JING-PIN;賴光啟;LAI, KUANG-CHI;郭秀滿;KUO, HSIU-MAAN;夏德椿;HSIA, TE-CHUN;鍾景光;Chung, Jing-Gung
    Contributors: 生物科技學系
    Keywords: "cantharidin;human bladder cancer TSGH 8301 cells;apoptosis;mitochondria"
    Date: 2010-11
    Issue Date: 2012-11-23 17:13:58 (UTC+8)
    Abstract: "Cantharidin has shown potent anticancer activities
    on many types of human cancer cells. This study was
    performed to elucidate whether mitochondria and caspases
    are involved in the modulation of apoptosis and cell cycle
    arrest by cantharidin in human bladder cancer cells. The
    effect of cantharidin on cell cycle arrest, apoptosis, caspases,
    reactive oxygen species (ROS) and mitochondrial membrane
    potential (Δæm) were measured by flow cytometry, and the
    levels of apoptosis-associated proteins and its regulatory
    molecules were studied by Western blotting. Cantharidininduced
    apoptosis and DNA damage was determined by
    flow cytometric analysis, DAPI staining and Comet assay.
    After cantharidin treatment, the active forms of caspase-3, -8
    and -9 were promoted. Cantharidin-induced apoptosis was
    associated with enhanced ROS and Ca2+ generations, caused
    DNA damage, decreased the levels of Δæm and promoted
    Endo G and AIF released from mitochondria. Cantharidininduced
    G0/G1 arrest was associated with a marked decrease
    in the protein expressions of cyclin E and Cdc25c but
    promoted the levels of p21 and p-p53. Cantharidin-induced
    apoptosis was accompanied with up-regulation of the protein
    expression of Bax and PARP, but down-regulation of the
    protein levels of Bcl-2, resulting in dysfunction of mitochondria
    then led to Endo G and AIF release for causing
    induction of apoptosis."
    Appears in Collections:[生物科技學系] 期刊論文

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