| First Author | Bugge TH | Year | 1997 |
| Journal | Blood | Volume | 90 |
| Issue | 11 | Pages | 4522-31 |
| PubMed ID | 9373263 | Mgi Jnum | J:44314 |
| Mgi Id | MGI:1099889 | Doi | 10.1182/blood.v90.11.4522 |
| Citation | Bugge TH, et al. (1997) Growth and dissemination of Lewis lung carcinoma in plasminogen-deficient mice. Blood 90(11):4522-31 |
| abstractText | 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. |
