Abstract
The role of ecto-5'-nucleotidase (CD73), an enzyme providing interstitial adenosine, was investigated in B16F10 melanoma progression. Chemical inhibition of CD73 decreased adherence of cells to extracellular matrix proteins in vitro and led to enhanced migration and invasion. Both processes were reversed by adenosine receptor agonists. In CD73‑deficient mice, tumor growth was decreased in comparison with that of wild-type animals. Additionally, the vasculature of CD73-inhibited tumors was impaired and neoangiogenesis in Matrigel plugs was reduced. It is, therefore, proposed that although CD73 shows anti-invasive and antimigratory function in B16F10 melanoma cells, its proangiogenic action is prevalent in vivo and may contribute to increased tumor growth.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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5'-Nucleotidase / antagonists & inhibitors*
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5'-Nucleotidase / biosynthesis
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5'-Nucleotidase / genetics
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Adenosine Diphosphate / analogs & derivatives
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Adenosine Diphosphate / pharmacology
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Animals
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Antigens, CD / biosynthesis
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Apyrase / biosynthesis
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Cell Adhesion
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Cell Line, Tumor
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Cell Movement
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Cell Proliferation
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Extracellular Matrix Proteins / metabolism
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HEK293 Cells
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Humans
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Melanoma, Experimental / pathology*
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Neoplasm Invasiveness / pathology*
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Neovascularization, Pathologic / genetics
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Neovascularization, Pathologic / pathology*
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Purinergic P1 Receptor Agonists / pharmacology
Substances
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Antigens, CD
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Extracellular Matrix Proteins
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Purinergic P1 Receptor Agonists
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alpha,beta-methyleneadenosine 5'-diphosphate
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Adenosine Diphosphate
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5'-Nucleotidase
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Apyrase
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CD39 antigen