Abstract
While protease-activated receptors (PARs) play a traditional role in vascular biology, they emerge with surprisingly new assignments in tumor biology. PAR1 expression correlates with the invasion properties of breast carcinoma, whereas human PAR1 antisense reduces their ability to migrate through Matrigel. Part of the molecular mechanism of PAR1 invasion involves the formation of focal contact complexes on PAR1 activation. PAR1 induces angiogenesis in animal models in vivo and exhibits an oncogenic phenotype of enhanced ductal complexity when overexpressed in mouse mammary glands.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Breast / blood supply
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Breast / growth & development
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology
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Cell Division
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Cytoskeleton / ultrastructure
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Epithelial Cells / metabolism*
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Epithelial Cells / pathology
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Female
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Humans
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Integrins / physiology
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Mice
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Mice, Knockout
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Morphogenesis
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Neoplasm Invasiveness / physiopathology*
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Neoplasm Metastasis / physiopathology*
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Neovascularization, Pathologic / physiopathology
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Oligonucleotides, Antisense / pharmacology
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Placenta / blood supply
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Pregnancy
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Receptor, PAR-1 / physiology*
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Receptors, Vitronectin / physiology
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Thrombin / physiology
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Vascular Endothelial Growth Factor A / biosynthesis
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Vascular Endothelial Growth Factor A / genetics
Substances
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Integrins
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Oligonucleotides, Antisense
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Receptor, PAR-1
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Receptors, Vitronectin
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Vascular Endothelial Growth Factor A
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integrin alphaVbeta5
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Thrombin