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Spontaneous lung and lymph node metastasis in transgenic breast cancer is independent of the urokinase receptor uPAR

På svenska

Author

  • Kasper Almholt
  • Ole Didrik Laerum
  • Boye Schnack Nielsen
  • Ida Katrine Lund
  • Leif Roge Lund
  • John Romer
  • Annika Jögi

Summary, in English

Urokinase-type plasminogen activator (uPA) is an extracellular protease that plays a pivotal role in tumor progression. uPA activity is spatially restricted by its anchorage to high-affinity uPA receptors (uPAR) at the cell surface. High tumor tissue expression of uPA and uPAR is associated with poor prognosis in lung, breast, and colon cancer patients in clinical studies. Genetic deficiency of uPA leads to a significant reduction in metastases in the murine transgenic MMTV-PyMT breast cancer model, demonstrating a causal role for uPA in cancer dissemination. To investigate the role of uPAR in cancer progression, we analyze the effect of uPAR deficiency in the same cancer model. uPAR is predominantly expressed in stromal cells in the mouse primary tumors, similar to human breast cancer. In a cohort of MMTV-PyMT mice [uPAR-deficient (n = 31) or wild type controls (n = 33)], tumorigenesis, tumor growth, and tumor histopathology were not significantly affected by uPAR deficiency. Lung and lymph node metastases were also not significantly affected by uPAR deficiency, in contrast to the significant reduction seen in uPA-deficient mice. Taken together, our data show that the genetic absence of uPAR does not influence the outcome of the MMTV-PyMT cancer model.

Department/s

Publishing year

2015

Language

English

Pages

543-554

Publication/Series

Clinical and Experimental Metastasis

Volume

32

Issue

6

Document type

Journal article

Publisher

Springer

Topic

  • Cancer and Oncology

Keywords

  • Metastasis
  • uPAR
  • Antibody
  • Mouse model
  • Breast cancer

Status

Published

ISBN/ISSN/Other

  • ISSN: 1573-7276