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    ASIA unversity > 管理學院 > 國際企業學系 > 期刊論文 >  Item 310904400/79683

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/79683

    Title: Syk/JNK/AP-1 Signaling Pathway Mediates Interleukin-6-Promoted Cell Migration in Oral Squamous Cell Carcinoma
    Authors: Jing-Yuan Chuang;Yuan-Li Huang;Wei-Lin Yen;I-Ping Chiang;Ming-Hsui Tsai;Chih-Hsin Tang
    Contributors: 生物科技學系
    Keywords: Interleukin-6 (IL-6);oral squamous cell carcinoma (OSCC);Intercellular adhesion molecule-1 (ICAM-1);Syk;c-Jun N-terminal kinase (JNK)
    Date: 2014-01
    Issue Date: 2014-06-05 11:52:51 (UTC+8)
    Abstract: Oral squamous cell carcinoma (OSCC) typically migrates and metastasizes. Interleukin-6 (IL-6) is a multifunctional cytokine associated with disease status and cancer outcomes. The effect of IL-6 on human OSCC cells, however, is unknown. Here, we showed that IL-6 increased cell migration and Intercellular adhesion molecule-1 (ICAM-1) expression in OSCC cells. Pretreatment of OSCC cells with IL-6R monoclonal antibody (mAb) significantly abolished IL-6-induced cell migration and ICAM-1 expression. By contrast, IL-6-mediated cell motility and ICAM-1 upregulation were attenuated by the Syk and c-Jun N-terminal kinase (JNK) inhibitors. Stimulation of OSCC cells with IL-6 promoted Syk and JNK phosphorylation. Furthermore, IL-6 enhanced AP-1 activity, and the IL-6R mAb, Syk inhibitor, or JNK inhibitor all reduced IL-6-mediated c-Jun phosphorylation, c-Jun binding to the ICAM-1 promoter, and c-Jun translocation into the nucleus. Our results indicate that IL-6 enhances the migration of OSCC cells by increasing ICAM-1 expression through the IL-6R receptor and the Syk, JNK, and AP-1 signal transduction pathways.
    Appears in Collections:[國際企業學系] 期刊論文

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