| First Author | Terraube V | Year | 2006 |
| Journal | J Thromb Haemost | Volume | 4 |
| Issue | 3 | Pages | 519-26 |
| PubMed ID | 16405520 | Mgi Jnum | J:135771 |
| Mgi Id | MGI:3794454 | Doi | 10.1111/j.1538-7836.2005.01770.x |
| Citation | Terraube V, et al. (2006) Increased metastatic potential of tumor cells in von Willebrand factor-deficient mice. J Thromb Haemost 4(3):519-26 |
| abstractText | BACKGROUND: The key role played by von Willebrand factor (VWF) in platelet adhesion suggests a potential implication in various pathologies, where this process is involved. In cancer metastasis development, tumor cells interact with platelets and the vessel wall to extravasate from the circulation. As a potential mediator of platelet-tumor cell interactions, VWF could influence this early step of tumor spread and therefore play a role in cancer metastasis. OBJECTIVES: To investigate whether VWF is involved in metastasis development. METHODS: In a first step, we characterized the interaction between murine melanoma cells B16-BL6 and VWF in vitro. In a second step, an experimental metastasis model was used to compare the formation of pulmonary metastatic foci in C57BL/6 wild-type and VWF-null mice following the injection of B16-BL6 cells or Lewis lung carcinoma cells. RESULTS: In vitro adhesion assays revealed that VWF is able to promote a dose-dependent adhesion of B16-BL6 cells via its Arg-Gly-Asp (RGD) sequence. In the experimental metastasis model, we found a significant increase in the number of pulmonary metastatic foci in VWF-null mice compared with the wild-type mice, a phenotype that could be corrected by restoring VWF plasma levels. We also showed that increased survival of the tumor cells in the lungs during the first 24 h in the absence of VWF was the cause of this increased metastasis. CONCLUSION: These findings suggest that VWF plays a protective role against tumor cell dissemination in vivo. Underlying mechanisms remain to be investigated. |
