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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16225

    Title: Endothelin-1 promotes MMP-13 production and migration in human chondrosarcoma cells through FAK/PI3K/Akt/mTOR pathways
    Authors: Min Huan Wu;Jeng-Fan Lo;Chia-Hua Kuo;James A. Lin;Yueh-Min Lin;Li-Mien Chen;Fuu-Jen Tsai;Chang-Hai Tsai;Chih-Yang Huang;Chih-Hsin Tang
    Contributors: 生物科技學系
    Date: 2012
    Issue Date: 2012-11-23 17:10:10 (UTC+8)
    Abstract: Tumor malignancy is associated with several cellular properties including proliferation and ability to metastasize. Endothelin-1 (ET-1) the most potent vasoconstrictor plays a crucial role in migration and metastasis of human cancer cells. We found that treatment of human chondrosarcoma (JJ012 cells) with ET-1 increased migration and expression of matrix metalloproteinase (MMP)-13. ET-1-mediated cell migration and MMP-13 expression were reduced by pretreatment with inhibitors of focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), Akt, and mammalian target of rapamycin (mTOR), as well as the NF-κB inhibitor and the IκB protease inhibitor. In addition, ET-1 treatment induced phosphorylation of FAK, PI3K, AKT, and mTOR, and resulted in increased NF-κB-luciferase activity that was inhibited by a specific inhibitor of PI3K, Akt, mTOR, and NF-κB cascades. Taken together, these results suggest that ET-1 activated FAK/PI3K/AKT/mTOR, which in turn activated IKKα/β and NF-κB, resulting in increased MMP-13 expression and migration in human chondrosarcoma cells.
    Relation: JOURNAL OF CELLULAR PHYSIOLOGY,227(8),3016–3026.
    Appears in Collections:[生物科技學系] 期刊論文

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