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Download Cancer metastatis, molecular and cellular mechanisms and by Wen G Jiang; R E Mansel PDF

By Wen G Jiang; R E Mansel

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Extra resources for Cancer metastatis, molecular and cellular mechanisms and clinical intervention

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SUBSTRATES Initially the MMPs were defined by their ability to degrade extracellular matrix and both MMP-2 and 9 fit that pattern with activity against denatured collagens of many types including collagens Type IV and V, elastin, gelatin, and fibronectin. More recently however a variety of additional non-matrix physiological targets have been identified including basic fibroblast growth factor, the cell surface protein galectin and a variety of proteins affecting inflammation. Specificity can be discerned.

Stack MS, Gately S, Bafetti LM, Enghild J, Soff GA. Angiostatin inhibitits endothelial and melanoma cellular invasion by blocking matrix-enhanced plasminogen activation. Biochem J 1999; 340: 77–84. Stahl A, Mueller BM. Melanoma cell migration on vitronectin: regulation by components of the plasminogen activation system. Int J Cancer 1997; 71: 116–122. Stefansson S, Lawrence DA. The serpin PAI-1 inhibits cell migration by blocking integrin alpha V beta 3 binding to vitronectin [see comments]. Nature 1996; 383: 441–443.

Tumor growth was unaffected (Bernhard et al, 1994). Similar experiments in melanoma cells also demonstrated the ability of MMP-9 to augment metastasis (MacDougall et al, 1999). In complementary experiments, downregulation of MMP-9 using a ribozyme, curtailed metastasis in a sarcoma model system or a prostatic carcinoma model, while this down regulation did not alter tumor growth rate (Hua and Muschel, 1996; Sehgal et al, 1998). Thus strong evidence exists demonstrating the importance of MMP-9 expression in tumor cells contributing to metastasis.

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