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Research Article Free access | 10.1172/JCI118323

Expression of plasminogen activator inhibitor type 1 by human prostate carcinoma cells inhibits primary tumor growth, tumor-associated angiogenesis, and metastasis to lung and liver in an athymic mouse model.

G A Soff, J Sanderowitz, S Gately, E Verrusio, I Weiss, S Brem, and H C Kwaan

Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Division of Hematology/Oncology, Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.

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Published December 1, 1995 - More info

Published in Volume 96, Issue 6 on December 1, 1995
J Clin Invest. 1995;96(6):2593–2600. https://doi.org/10.1172/JCI118323.
© 1995 The American Society for Clinical Investigation
Published December 1, 1995 - Version history
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Abstract

Expression of urokinase-type plasminogen activator (uPA) by malignant cells correlates with an aggressive phenotype, including increased invasiveness, tumor-associated angiogenesis, and metastases. Plasminogen activator inhibitor type 1 (PAI-1) is undetectable in cells of some aggressive malignancies, but present in the stroma of tumor-associated microvasculature. This analysis of an athymic mouse model of prostate carcinoma further defines the role of the uPA/PAI-1/plasmin system in primary growth and metastasis. A marked increase in PAI-1 expression was induced in clones of the aggressive human prostate carcinoma line, PC-3, by stable transfection. Primary PC-3 tumors, in mice, were significantly smaller when derived from PAI-1 expressing versus control cells. PAI-1 expression reduced the density of tumor-associated microvasculature by 22-38%. Microscopic metastases were quantitated using stable expression of the chromogenic label (beta-galactosidase) in control and PAI-1 expressing cells. PAI-1 expression resulted in a significant inhibition of lung metastases, and liver metastases. Expression of PAI-1 by malignant prostate cells resulted in a less aggressive phenotype, presumably by inhibition of uPA activity, suggesting pharmacologic or molecular inhibition of uPA activity as a potential therapeutic target.

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