Polyoma middle T-induced vascular tumor formation: the role of the plasminogen activator/plasmin system.

Détails

ID Serval
serval:BIB_878CA1648284
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Polyoma middle T-induced vascular tumor formation: the role of the plasminogen activator/plasmin system.
Périodique
Journal of Cell Biology
Auteur(s)
Sabapathy K.T., Pepper M.S., Kiefer F., Möhle-Steinlein U., Tacchini-Cottier F., Fetka I., Breier G., Risau W., Carmeliet P., Montesano R., Wagner E.F.
ISSN
0021-9525 (Print)
ISSN-L
0021-9525
Statut éditorial
Publié
Date de publication
1997
Volume
137
Numéro
4
Pages
953-963
Langue
anglais
Résumé
The middle T antigen of murine Polyomavirus (PymT) rapidly transforms endothelial cells, leading to the formation of vascular tumors in newborn mice. Transformed endothelial (End.) cell lines established from such tumors exhibit altered proteolytic activity as a result of increased expression of urokinase-type plasminogen activator (uPA) and are capable of inducing vascular tumors efficiently when injected into adult mice. In this study we have used mice lacking components of the PA/plasmin system to analyze the role of this system in the transformation process and in tumor growth. We found that the proteolytic status of the host is not a critical determinant for PymT-induced vascular tumor formation. In addition, the lack of either uPA or tissue-type PA (tPA) activity is not limiting for the establishment and proliferation of End. cells in vitro, although the combined loss of both PA activities leads to a marked reduction in proliferation rates. Furthermore, the in vitro morphogenetic properties of mutant End. cells in fibrin gels could only be correlated with an altered proteolytic status in cells lacking both uPA and tPA. However, in contrast with tumors induced by PymT itself, the tumorigenic potential of mutant and wild-type End. cell lines was found to be highly dependent on the proteolytic status of both the tumor cells and the host. Thus, genetic alterations in the PA/plasmin system affect vascular tumor development, indicating that this system is a causal component in PymTmediated oncogenesis.
Mots-clé
Animals, Animals, Newborn, Antigens, Polyomavirus Transforming, Cell Line, Cell Transformation, Viral, Endothelium, Vascular/cytology, Endothelium, Vascular/enzymology, Fibrin, Fibrinolysin/physiology, Gels, Gene Expression, Mice, Mice, Knockout, Morphogenesis, Plasminogen Activator Inhibitor 1/deficiency, Plasminogen Activators/physiology, RNA, Messenger/genetics, Tissue Plasminogen Activator/deficiency, Urokinase-Type Plasminogen Activator/deficiency, Vascular Neoplasms/etiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 16:08
Dernière modification de la notice
08/05/2019 21:29
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