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Growth and Dissemination of Lewis Lung Carcinoma in Plasminogen-Deficient Mice
Thomas H. Bugge,
Keith W. Kombrinck,
Qing Xiao,
Kenn Holmbäck,
Cynthia C. Daugherty,
Dave P. Witte, and
Jay L. Degen
From the Divisions of Developmental Biology and Pathology, Children's Hospital Research Foundation, Cincinnati, OH.
Plasminogen activation has been proposed to play a critical role in cancer invasion and metastasis. The effects of complete ablation of plasminogen activation in cancer was studied by inoculation of a metastatic Lewis lung carcinoma expressing high levels of plasminogen activator into plasminogen-deficient (Plg-/-) mice and matched control mice. Primary tumors developed in all mice with no difference in the rate of appearance between Plg-/- and control mice. However, the primary tumors in Plg-/- mice were smaller and less hemorrhagic and displayed reduced skin ulceration. In addition, dissemination of the tumor to regional lymph nodes was delayed in Plg-/- mice. Surprisingly, no quantitative differences were observed in lung metastasis between Plg-/- and control mice. In addition, Plg deficiency was compatible with metastasis of the primary tumor to a variety of other organs. Nevertheless, Plg-/- mice displayed a moderately increased survival after primary tumor resection. These findings suggest that plasmin-mediated proteolysis contributes to the morbidity and mortality of Lewis lung carcinoma in mice, but sufficient proteolytic activity is generated in Plg-/- mice for efficient tumor development and metastasis.
Blood, Vol. 90 No. 11 (December 1), 1997:
pp. 4522-4531
© 1997 by The American Society of Hematology.
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