A possible explanation of mechanisms inducing inhibition of vascularization of tumours by antifibrinolytic drugs--the influence of migratory behaviour of endothelial cells.
The observation that administration of antifibrinolytic drugs results in tumour growth stasis, having possibly its origin in reduced vascularization of the tumour, led us to investigate the migratory behaviour of bovine endothelial cells under in vitro conditions in the presence of drugs known to influence the activity of fibrinolytic enzymes. The Boyden-technique and microcinematography were used for this analysis. It could be shown that aprotinin, an inhibitor of serine proteinases and para-methylaminobenzoic acid, a specific inhibitor of plasminogen activation and plasmin action greatly reduced the migratory rate of the cells. Streptokinase, a plasminogen activator, stimulated the cell migration in optimal concentrations. The authors hypothesize that tumour vascularization is initiated by immigration of endothelial cells into the tumour by fibrinolytic action following a fibrin gradient induced by the tumour themselves. Fibrinolytic inhibitors suppress this process.
D010129:4-Aminobenzoic Acid / Q000494:pharmacology; D000818:Animals; D000933:Antifibrinolytic Agents / Q000494:pharmacology*; D001011:Aorta / Q000166:cytology*; D007611:Aprotinin / Q000494:pharmacology; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D002642:Chick Embryo; D004727:Endothelium / Q000166:cytology*; D009369:Neoplasms / Q000098:blood supply*; D009389:Neovascularization, Pathologic; D013300:Streptokinase / Q000494:pharmacology; D062366:para-Aminobenzoates
D000933:Antifibrinolytic Agents; D062366:para-Aminobenzoates; C015668:4-aminomethylbenzoic acid; D007611:Aprotinin; D013300:Streptokinase; D010129:4-Aminobenzoic Acid