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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/17046


    Title: Chlorella sorokiniana induces mitochondrial-mediated apoptosis in human non-small cell lung cancer cells and inhibits xenograft tumor growth in vivo
    Authors: Lin, P.-Y.
    Tsai, C.-T.
    Chuang, W.-L.
    Chao, Y.-H.
    Pan, I.-H.
    Chen, Y.-K.
    Lin, C.-C.
    Wang, B.-Y.
    Contributors: 醫學系
    Keywords: Chlorella sorokiniana;Human non-small cell lung cancer cells;Mitochondrial apoptotic pathway
    Date: 2017-02
    Issue Date: 2017-02-14T08:09:26Z (UTC)
    Publisher: BioMed Central Ltd.
    ISSN: 1472-6882
    Abstract: Background: Lung cancer is one of the leading causes of cancer related deaths worldwide. Marine microalgae are a source of biologically active compounds and are widely consumed as a nutritional supplement in East Asian countries. It has been reported that Chlorella or Chlorella extracts have various beneficial pharmacological compounds that modulate immune responses; however, no studies have investigated the anti-cancer effects of Chlorella sorokiniana (CS) on non-small cell lung cancer (NSCLC). Methods: In this study, we evaluated the anti-cancer effects of CS in two human NSCLC cell lines (A549 and CL1-5 human lung adenocarcinoma cells), and its effects on tumor growth in a subcutaneous xenograft tumor model. We also investigated the possible molecular mechanisms governing the pharmacological function of CS. Results: Our results showed that exposure of the two cell lines to CS resulted in a concentration-dependent reduction in cell viability. In addition, the percentage of apoptotic cells increased in a dose-dependent manner, suggesting that CS might induce apoptosis in human NSCLC cells. Western blot analysis revealed that exposure to CS resulted in increased protein expression of the cleaved/activated forms of caspase-3, caspase-9, and PARP, except caspase-8. ZDEVD (caspase-3 inhibitor) and Z-LEHD (caspase-9 inhibitor) were sufficient at preventing apoptosis in both A549 and CL1-5 cells, proving that CS induced cell death via the mitochondria-mediated apoptotic pathway. Exposure of A549 and CL1-5 cells to CS for 24h resulted in decreased expression of Bcl-2 protein and increased expression of Bax protein as well as decreased expression of two IAP family proteins, survivin and XIAP. Conclusions: We demonstrated that CS induces mitochondrial-mediated apoptosis in NSCLC cells via downregulation of Bcl-2, XIAP and survivin. In addition, we also found that the tumors growth of subcutaneous xenograft in vivo was markedly inhibited after oral intake of CS.
    URI: http://dx.doi.org/10.1186/s12906-017-1611-9
    https://ir.csmu.edu.tw:8080/ir/handle/310902500/17046
    Relation: BMC Complementary and Alternative Medicine,Volume 17, Issue 1, 1 February 2017, 論文編號 88
    Appears in Collections:[醫學系] 期刊論文

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