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Wen G Jiang; R E Mansel's Cancer metastatis, molecular and cellular mechanisms and PDF

By Wen G Jiang; R E Mansel

ISBN-10: 0306483882

ISBN-13: 9780306483882

ISBN-10: 0792363957

ISBN-13: 9780792363958

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

Sample text

2. system Other uPA effects independent of its plasminogen activating function include growth factor-like function, chemotactic, adhesive and migratory properties [for review, see (Blasi, 1997; Chapman et al, 1999)]. Most of these functions are mediated by binding of uPA to its cell surface receptor. uPA conveys a mitogenic signal, probably by several ways. Inactive forms of this enzyme or even ATF stimulate the proliferation of osteosarcoma cells (Rabbani et al, 1990) or ovarian carcinoma cells (Fischer et al, 1998).

Chapman et al (1999) have identified a peptide able to disrupt uPAR-caveolin integrin complexes. Thus, the cholesterol binding protein termed caveolin associates with β1 integrins. This association is required for src-kinases binding β1 integrins. In the presence of the peptide that disrupts the uPARcaveolin-β1 integrin, there is a loss of focal adhesion kinase phosphorylation and no formation of focal adhesion sites (Chapman et al, 1999). 4. TARGETED GENE-INACTIVATION Recent studies using gene-deficient mice focused on the contribution of host uPA, tPA, uPAR, plasminogen and PAI-1 in tumor growth, angiogenesis and dissemination.

On the contrary, uPA mediated stimulation of smooth muscle cell proliferation requires its enzymatic activity. It appears therefore that several mitogenic signals can be switched on by uPA and that different parts of the uPA molecule may be involved depending upon cell type and mechanisms [for a review, see (Schmitt et al, 2000)]. The uPAR is a true chemotactic molecule whose activity lies within the protease-sensitive region linking domains 1 and 2 of uPAR, which can be cleaved by uPA. Synthetic peptides spanning this epitope promote chemotaxis and activate P56/p59 hck tyrosine kinase.

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Cancer metastatis, molecular and cellular mechanisms and clinical intervention by Wen G Jiang; R E Mansel


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