Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis
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Hanahan, D. & Folkman, J. Patterns and emerging mechanisms of the angiogenic switch during tumourigenesis. Cell 86, 353–364 (1996).
Bouck, N., Stellmach, V. & Hsu, S. C. How tumours become angiogenic. Adv. Cancer Res. 69, 135–174 (1996).
Hanahan, D. Heritable formation of pancreatic β-cell tumours in transgenic mice harboring recombinant insulin/simian virus 40 oncogenes. Nature 315, 115–122 (1985).
Folkman, J., Watson, K., Ingber, D. & Hanahan, D. Induction of angiogenesis during the transition from hyperplasia to neoplasia. Nature 339, 58–61 (1989).
Dvorak, H. F., Nagy, J. A., Feng, D., Brown, L. F. & Dvorak, A. M. Vascular permeability factor/vascular endothelial growth factor and the significance of microvascular hyperpermeability in angiogenesis. Curr. Top. Microbiol. Immunol. 237, 97–132 (1999).
Kerbel, R. S., Viloria-Petit, A., Okada, F. & Rak, J. Establishing a link between oncogenes and tumour angiogenesis. Mol. Med. 4, 286–295 (1998).
Faller, D. V. Endothelial cell responses to hypoxic stress. Clin. Exp. Pharmacol. Physiol. 26, 74–84 (1999).
Hanahan, D., Christofori, G., Naik, P. & Arbeit, J. Transgenic mouse models of tumour angiogenesis: the angiogenic switch, its molecular controls, and prospects for preclinical therapeutic models. Eur. J. Cancer 32A, 2386–2393 (1996).
Christofori, G., Naik, P. & Hanahan, D. Vascular endothelial growth factor and its receptors, flt-1 and flk-1, are expressed in normal pancreatic islets and throughout islet cell tumourigenesis. Mol. Endocrinol. 9, 1760–1770 (1995).
Roberts W. G. & Palade, G. E. Neovasculature induced by vascular endothelial growth factor is fenestrated. Cancer Res. 57, 765–72 (1997).
Vajkoczy, P. et al. Inhibition of tumour growth, angiogenesis, and microcirculation by the novel flk-1 inhibitor SU5416 as assessed by intravital multi-fluorescence videomicroscopy. Neoplasia 1, 31–41 (1999).
Brekken, R. A., Huang, X., King, S. W. & Thorpe, P. E. Vascular endothelial growth factor as a marker of tumour endothelium. Cancer Res. 58, 1952–1959 (1998).
Cheng, S. Y., Nagane, M., Huang, H. S. & Cavenee, W. K. Intracerebral tumour-associated hemorrhage caused by overexpression of the vascular endothelial growth factor isoforms VEGF121 and VEGF165 but not VEGF189. Proc. Natl Acad. Sci. USA 94, 12081–12087 (1997).
Ferrara, N. et al. Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene. Nature 380, 439–442 (1996).
Carmeliet, P. et al. Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele. Nature 380, 435–439 (1996).
O'Reilly, M. S., Widerschain, D., Stetler-Stevenson, W. G., Folkman, J. & Moses, M. A. Regulation of angiostatin production by matrix metalloproteinase-2 in a model of concomitant resistance. J. Biol. Chem. 274, 29568–29571 (1999).
Talbot, D. C. & Brown, P. D. Experimental and clinical studies on the use of matrix metalloprotease inhibitors for the treatment of cancer. Eur. J. Cancer 32A, 2528–2533. (1996).
Brown, P. D. Clinical studies with matrix metalloprotease inhibitors. Acta Pathologica Microbiologica et Immunologica Sacndinavica 107, 174–80 (1999).
Tamaki, K. et al. Synthesis and structure–activity relationships of gelatinase inhibitors derived from matlystatins. Chem. Pharmaceut. Bull. 43, 1883–1893 (1995).
Bergers, G., Javaherian, K., Lo, K-M., Folkman, J. & Hanahan, D. Differential effects of angiogenesis inhibitors on distinct stages of carcinogenesis. Science 284, 808–812 (1999).
Vu, T.H. et al. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. Cell 93, 411–422 (1998).
Itoh, T. et al. Unaltered secretion of beta-amyloid precursor protein in gelatinase A (matrix metalloprotease 2)-deficient mice. J. Biol. Chem. 272, 22389–22392 (1997).
Itoh, T. et al. Reduced angiogenesis and tumour progression in gelatinase A-deficient mice. Cancer Res. 58, 1048–1051 (1998).
Carmeliet, P. et al. Urokinase-generated plasmin activates matrix metalloproteinases during aneurysm formation. Nature Gen. 17, 439–444 (1997).
Vlodavsky, I. et al. Extracellular matrix-resident growth factors and enzymes: possible involvement in tumour metastasis and angiogenesis. Cancer Metastasis Rev., 9, 203–226 (1990).
Hulett, M. D. et al. Cloning of mammalian heparanase, an important enzyme in tumour invasion and metastasis. Nature Med. 7, 803–809 (1999).
Vlodavsky, I. et al. Mammalian heparanase: gene cloning, expression and function in tumour progression and metastasis. Nature Med. 7, 793–802 (1999).
Coussens, L. M. et al. Inflammatory mast cells upregulate angiogenesis during squamous epithelial carcinogenesis. Genes Dev. 13, 1382–1397 (1999).
Gerber, H-P. et al. VEGF couples hypertrophic cartilage remodeling, ossification and angiogenesis during endochondral bone formation. Nature Med. 5, 623–628 (1999).
Coussens, L. M., Tinkle, C. L., Hanahan, D. & Werb, Z. MMP-9 supplied by bone marrow-derived cells contributes to skin carcinogenesis. Cell (in the press).
Zucker, S. et al. Measurement of matrix metalloprotease and tissue inhibitors of metalloproteinases in blood and tissues. Clinical and experimental applications. Ann. NY Acad. Sci. 878, 212–227 (1999).
Fang, J. et al. Matrix metalloproteinase-2 is required for the switch to the angiogenic phenotype in a tumour model. Proc. Natl Acad. Sci. USA 97, 3884–3889 (2000).
Zhou, Z. et al. Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I. Proc. Natl Acad. Sci. USA 97, 4052–4057 (2000).
Yu, Q. & Stamenkovic, I. Cell surface-localized metalloproteinase-9 proteolyically activates TGF-beta and promotes tumour invasion and angiogenesis. Genes Dev. 14, 163–176 (2000).
Perl, A. K. et al. A causal role for E-cadherin in the transition from adenoma to carcinoma. Nature 392, 190–193 (1998).
Behrendtsen, O., Alexander, C. M. & Werb, Z. Metalloproteinases mediate extracellular matrix degradation by cells from mouse blastocyst outgrowths. Development 114, 447–456 (1992).
Naik, P., Karrim, J. & Hanahan, D. The rise and fall of apoptosis during multistage tumourigenesis: downmodulation contributes to progression from angiogenic progenitors. Genes Dev. 10, 2105–2116 (1996).
Herron, G. S., Werb, Z., Dwyer, K. & Banda, M. J. Secretion of metalloproteinases by stimulated capillary endothelial cells. I. Production of procollagenases and prostromelysin exceeds expression of proteolytic activity. J. Biol. Chem. 261, 2810–2813 (1986).
Herron, G. S., Banda, M. J., Clark, E. J., Gavrilovic, J. & Werb, Z. Secretion of metalloproteinases by stimulated capillary endothelial cells. II. Expression of collagenase and stromelysin activities is regulated by endogenous inhibitors. J. Biol. Chem. 261, 2814–2818 (1986).
Talhouk, R. S., Chin, J. R., Unemori, E. N., Werb, Z. & Bissell, M. J. Proteinases of the mammary gland: developmental regulation in vivo and vectorial secretion in culture. Development 112, 439–449 (1991).
Parangi, S., Dietrich, W., Christofori, G., Lander, E. S. & Hanahan, D. Tumour suppressor loci on mouse chromosomes 9 and 16 are lost at distinct stages of tumourigenesis in a transgenic model of islet cell carcinoma. Cancer Res. 55, 6071–6076 (1995).