By Wen G Jiang; R E Mansel
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Extra info for Cancer metastatis, molecular and cellular mechanisms and clinical intervention
Oncogene 1998; 16: 3097–3104. Carmeliet P, Collen D. Development and disease in proteinase-deficient mice: role of the plasminogen, matrix metalloproteinase and coagulation system. Thromb Res 1998; 91: 255–285. Carmeliet P, Moons L, Lijnen R, Baes M, Lemaitre V, Tipping P, Drew A, Eeckhout Y, Shapiro S, Lupu F, Collen D. Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation. Nat Genet 1997; 17: 439–444. Chambers SK, Gertz RE, Ivins CM, Kacinski BM. The significance of urokinase-type plasminogen 34 activator, its inhibitors and its receptor in ascites of patients with epithelial ovarian cancer.
Primary Lewis lung carcinomas developed both in wild-type and plasminogen –/– mice (Bugge et al, 1997). However, dissemination of such tumors to regional lymph node was delayed in plasminogen–/– mice. Nevertheless, sufficient proteolytic activity is generated in plasminogen–/– mice for efficient tumor development and metastasis. Consistently, tumor vascularization was delayed but not completely impaired in plasminogen–/– mice transplanted with transformed keratinocytes (Bajou et al, 2001). Altogether, these data suggest that plasmin-mediated 29 proteolysis is essential, but not sufficient for tumor growth and angiogenesis.
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.
Cancer metastatis, molecular and cellular mechanisms and clinical intervention by Wen G Jiang; R E Mansel