Abstract
Receptor-bound urokinase is likely to be a crucial determinant in both tumor invasion and angiogenesis. We report here that a yeast-derived genetic conjugate between human serum albumin and the 1-135 N-terminal residues of urokinase (u-PA) competitively inhibits the binding of exogenous and endogenous u-PA to its cell-anchored receptor (u-PAR). This hybrid molecule (ATF-HSA) also inhibits in vitro pro-urokinase-dependent plasminogen activation in the presence of u-PAR bearing cells. These effects are probably responsible for the observed in vitro inhibition of tumor cell invasion in a reconstituted basement membrane extract (Matrigel).
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Cell Line
-
Cloning, Molecular
-
Humans
-
Kluyveromyces / genetics
-
Peptide Fragments / genetics
-
Peptide Fragments / pharmacology
-
Plasminogen / antagonists & inhibitors*
-
Receptors, Cell Surface / antagonists & inhibitors*
-
Receptors, Urokinase Plasminogen Activator
-
Recombinant Fusion Proteins / pharmacology
-
Saccharomyces cerevisiae / genetics
-
Serum Albumin / genetics
-
Serum Albumin / pharmacology*
-
Tumor Cells, Cultured
-
Urokinase-Type Plasminogen Activator / genetics
-
Urokinase-Type Plasminogen Activator / pharmacology*
Substances
-
PLAUR protein, human
-
Peptide Fragments
-
Receptors, Cell Surface
-
Receptors, Urokinase Plasminogen Activator
-
Recombinant Fusion Proteins
-
Serum Albumin
-
Plasminogen
-
Urokinase-Type Plasminogen Activator