Please use this identifier to cite or link to this item:
|標題:||Cyr61 increases migration and MMP-13 expression via alpha v beta 3 integrin, FAK, ERK and AP-1-dependent pathway in human chondrosarcoma cells||作者:||Tan, T.W.
|關鍵字:||growth-factor;signaling pathways;breast-cancer;matrix;metalloproteinases;tumor progression;up-regulation;lung-cancer;ccn;family;invasion;transduction||Project:||Carcinogenesis||期刊/報告no：:||Carcinogenesis, Volume 30, Issue 2, Page(s) 258-268.||摘要:||
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 effect of Cyr61 on migration activity in human chondrosarcoma cells is mostly unknown. Here, we found that Cyr61 increased the migration and expression of matrix metalloproteinase (MMP)-13 in human chondrosarcoma cells (JJ012 cells). RGD peptide, alpha v beta 3 monoclonal antibody and mitogen-activated protein kinase (MEK) inhibitors (PD98059 and U0126) but not RAD peptide inhibited the Cyr61-induced increase of the migration and MMP-13 upregulation of chondrosarcoma cells. Cyr61 stimulation increased the phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK). In addition, activator protein-1 (AP-1) decoy oligodeoxynucleotide also suppressed the MMP-13 messenger RNA and enzyme activity enhanced by Cyr61. Moreover, Cyr61 increased the binding of c-Fos and c-Jun to the AP-1 element on the MMP-13 promoter. Taken together, our results indicated that Cyr61 enhances the migration of chondrosarcoma cells by increasing MMP-13 expression through the alpha v beta 3 integrin receptor, FAK, ERK, c-Fos/c-Jun and AP-1 signal transduction pathway.
|Appears in Collections:||期刊論文|
Show full item record
TAIR Related Article
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.