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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/64322

    Title: AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma
    Authors: Chin-Jung Hsu;Min-Huan Wu;Chin-Yuan Chen;Chun-Hao Tsai;Horng-Chaung Hsu;Chih-Hsin Tang
    Contributors: 生物科技學系
    Keywords: CCL3;Chondrosarcoma;AMPK;MMP-2;CCR5
    Date: 2013-09
    Issue Date: 2013-10-29 17:37:11 (UTC+8)
    Abstract: Chemokine (C-C motif) ligand 3 (CCL3), also known as macrophage inflammatory protein-1alpha, is a cytokine involved in inflammation and activation of polymorphonuclear leukocytes. CCL3 has been detected in infiltrating cells and tumor cells. Chondrosarcoma is a highly malignant tumor that causes distant metastasis. However, the effect of CCL3 on human chondrosarcoma metastasis is still unknown. Here, we found that CCL3 increased cellular migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. Pre-treatment of cells with the MMP-2 inhibitor or transfection with MMP-2 specific siRNA abolished CCL3-induced cell migration. CCL3 has been reported to exert its effects through activation of its specific receptor, CC chemokine receptor 5 (CCR5). The CCR5 and AMP-activated protein kinase (AMPK) inhibitor or siRNA also attenuated CCL3-upregulated cell motility and MMP-2 expression. CCL3-induced expression of MMP-2 and migration were also inhibited by specific inhibitors, and inactive mutants of AMPK, p38 mitogen activated protein kinase (p38 or p38-MAPK), and nuclear factor kappaB (NF-kappaB) cascades. On the other hand, CCL3 treatment demonstrably activated AMPK, p38, and NF-kappaB signaling pathways. Furthermore, the expression levels of CCL3, CCR5, and MMP-2 were correlated in human chondrosarcoma specimens. Taken together, our results indicate that CCL3 enhances the migratory ability of human chondrosarcoma cells by increasing MMP-2 expression via the CCR5, AMPK, p38, and NF-kappaB pathways.
    Relation: Cell Communication and Signaling,11(1):68.
    Appears in Collections:[生物科技學系] 期刊論文

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