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|標題:||Cyr61 increases matrix metalloproteinase-3 expression and cell motility in human oral squamous cell carcinoma cells||作者:||Chuang, J.Y.
|關鍵字:||Cyr61;MIGRATION;OSCC;FAK;NF-?B;nf-kappa-b;adhesion molecules;cancer progression;growth-factor;integrin;phosphorylation;pathway;gene;differentiation;involvement||Project:||Journal of Cellular Biochemistry||期刊/報告no：:||Journal of Cellular Biochemistry, Volume 113, Issue 6, Page(s) 1977-1986.||摘要:||
Oral squamous cell carcinoma (OSCC) has a striking tendency to migrate and metastasize. Cysteine-rich 61 (Cyr61), from the CCN gene family, is a secreted and matrix-associated protein, which is involved in many cellular activities such as growth and differentiation. However, the effects of Cyr61 on human OSCC cells are largely unknown. In this study, we found that Cyr61 increased the migration and the expression of matrix metalloproteinases-3 (MMP)-3 in human OSCC cells. av beta 5 or a6 beta 1 monoclonal antibody (mAb), focal adhesion kinase (FAK) inhibitor, and mitogen-activated protein kinase (MEK) inhibitors (PD98059 and U0126) inhibited the Cyr61-induced increase of the migration and MMP-3 up-regulation of OSCC cells. Cyr61 stimulation increased the phosphorylation of FAK, MEK, and extracellular signal-regulated kinase (ERK). In addition, NF-?B inhibitors suppressed the cell migration and MMP-3 expression enhanced by Cyr61. Moreover, Cyr61 increased NF-?B luciferase activity and binding of p65 to the NF-?B element on the MMP-3 promoter. Taken together, our results indicate that Cyr61 enhances the migration of OSCC cells by increasing MMP-3 expression through the av beta 3 or a6 beta 1 integrin receptor, FAK, MEK, ERK, and NF-?B signal transduction pathway. J. Cell. Biochem. 113: 19771986, 2012. (C) 2012 Wiley Periodicals, Inc.
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