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Matrix metalloproteinases (MMPs) are essential for proper extracellular matrix remodeling. We previously found that a membrane-anchored glycoprotein, RECK, negatively regulates MMP-9 and inhibits tumor invasion and metastasis. Here we show that RECK regulates two other MMPs, MMP-2 and MT1-MMP, known to be involved in cancer progression, that mice lacking a functional RECK gene die around E10.5 with defects in collagen fibrils, the basal lamina, and vascular development, and that this phenotype is partially suppressed by MMP-2 null mutation. Also, vascular sprouting is dramatically suppressed in tumors derived from RECK-expressing fibrosarcoma cells grown in nude mice. These results support a role for RECK in the regulation of MMP-2 in vivo and implicate RECK downregulation in tumor angiogenesis.

Original publication

DOI

10.1016/s0092-8674(01)00597-9

Type

Journal article

Journal

Cell

Publication Date

12/2001

Volume

107

Pages

789 - 800

Addresses

Department of Molecular Oncology, Kyoto University Graduate School of Medicine, 606-8501, Kyoto, Japan.

Keywords

Muscle, Smooth, Vascular, Cells, Cultured, Tumor Cells, Cultured, Extracellular Matrix, Animals, Humans, Mice, Mice, Nude, Neoplasms, Experimental, Neovascularization, Pathologic, Metalloendopeptidases, Matrix Metalloproteinases, Membrane Glycoproteins, Immunohistochemistry, Gene Targeting, Transfection, Neoplasm Transplantation, Down-Regulation, Neovascularization, Physiologic, Mutation, Matrix Metalloproteinases, Membrane-Associated, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Matrix Metalloproteinase 14, Embryo, Mammalian, GPI-Linked Proteins