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    Please use this identifier to cite or link to this item: http://ir.meiho.edu.tw/ir/handle/987654321/3156


    Title: Sinularin Induces Apoptosis through Mitochondria Dysfunction and Inactivation of the pI3K/Akt/mTOR Pathway in Gastric Carcinoma Cells
    Authors: Yu-JenWu;Bing-Sang Wong;Shu-Hao Yea;Chi-I Lu;Shun-Hsiang Weng
    Keywords: sinularin;gastric cancer;apoptosis;mitochondrial dysfunction
    Date: 2016
    Issue Date: 2016-09-21T01:48:28Z (UTC)
    Abstract: Sinularin is an active compound isolated from the cultured soft coral Sinularia flexibilis. In this study, we investigated the effects of sinularin on two human gastric cancer cell lines, AGS and NCI-N87. Our results demonstrated that sinularin suppressed the proliferation of gastric cancer cells in a dose-dependent manner and induced apoptosis. In addition, the loss of mitochondrial membrane potential, the release of cytochrome C, the activation of Bax, Bad and caspase-3/9, and the suppression of p-Bad, Bcl-xL and Bcl-2 were observed in the cells treated with sinularin. This finding suggests that sinularin-induced apoptosis is associated with mitochondria-mediated apoptosis and occurs through caspase-dependent pathways. Furthermore, sinularin inhibited the phosphoinositol 3-kinase/Akt/mechanistic target of the rapamycin signaling pathway. Taken together, our results show that sinularin-induced apoptosis is mediated by activation of the caspase cascade and mitochondrial dysfunction. Our findings suggest that sinularin merits further evaluation as a chemotherapeutic agent for human gastric cancer.
    Relation: Drugs 2016, 14, 142; doi:10.3390/md14080142
    Appears in Collections:[Department of Food Science and Nutrition] Papers

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