Reference : Regulation of cancer invasion and vascularization by plasminogen activator inhibitor-1
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/37020
Regulation of cancer invasion and vascularization by plasminogen activator inhibitor-1
English
Noël, Agnès mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie cellulaire et moléculaire appliquée à l'homme >]
Bajou, Khalid mailto [Université de Liège - ULg > Département des sciences de la vie > GIGA-R : Biologie et génétique moléculaire >]
Masson, Véronique [Université de Liège - ULg > > Gynécologie-Obstétrique CHR >]
Frankenne, F. [ > > ]
Rakic, Jean-Marie mailto [Université de Liège - ULg > Département des sciences cliniques > Ophtalmologie >]
Lambert, Vincent mailto [Université de Liège - ULg > > Ophtalmologie >]
Carmeliet, P. [ > > ]
Foidart, Jean-Michel mailto [Université de Liège - ULg > Département des sciences cliniques > Gynécologie - Obstétrique - Labo de biologie des tumeurs et du développement >]
1999
Fibrinolysis and Proteolysis
Harcourt Publishers Ltd
13
6
220-225
Yes
International
1369-0191
[en] Acquisition of invasive/metastatic potential through protease expression is a key event in tumor progression. The proteolytic enzyme plasmin is generated from the precursor plasminogen by the action of urokinase-type plasminogen activator (urokinase, uPA) or tissue-type plasminogen activator (tPA). Plasminogen activator inhibitor-1 or PAI-1 is the main inhibitor of uPA and tPA. High levels of components of this proteolytic system, including uPA and its cell surface receptor (uPAR), have been correlated with a poor prognosis for different cancers. It was therefore anticipated that PAI-1 expression would be associated with favorable outcome. Paradoxically, high rather than low PAI-1 levels predict poor survival of patients suffering from a variety of cancers. Recent observations indicate a much more complex role of PAI-1 in tumor progression and angiogenesis than initially expected. The exact mechanisms of this multifunctional molecule remain puzzling.
http://hdl.handle.net/2268/37020
10.1054/fipr.2000.0043

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