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CCN3 increases cell motility and MMP-13 expression in human chondrosarcoma through integrin-dependent pathway

✍ Scribed by Huey-En Tzeng; Jui-Ching Chen; Chun-Hao Tsai; Chien-Chung Kuo; Horng-Chaung Hsu; Wen-Lee Hwang; Yi-Chin Fong; Chih-Hsin Tang

Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
526 KB
Volume
226
Category
Article
ISSN
0021-9541

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✦ Synopsis

Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. CCN3, also called nephroblastoma overexpressed gene (NOV), regulates proliferation and differentiation of cancer cells. However, the effect of CCN3 on migration activity in human chondrosarcoma cells is mostly unknown. Here, we found that CCN3 increased the migration and expression of matrix metalloproteinase (MMP)-13 in human chondrosarcoma cells (JJ012 cells). avb3 or avb5 monoclonal antibody (mAb), phosphatidylinositol 3-kinase (PI3K) inhibitors (Ly294002 and wortmannin) and Akt inhibitor inhibited the CCN3-induced increase of the migration and MMP-13 upregulation of chondrosarcoma cells. CCN3 stimulation increased the phosphorylation of focal adhesion kinase (FAK), PI3K, and Akt. In addition, NF-kB inhibitors also suppressed the cell migration and MMP-13 expression enhanced by CCN3. Moreover, CCN3 increased NF-kB luciferase activity and binding of p65 to the NF-kB element on the MMP-13 promoter. Taken together, our results indicate that CCN3 enhances the migration of chondrosarcoma cells by increasing MMP-13 expression through the avb3/avb5 integrin receptor, FAK, PI3K, Akt, p65, and NF-kB signal transduction pathway.

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