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Updated: Dec 4, 2025

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
Published on: August 14, 2017
von Willebrand factor promotes platelet-induced metastasis of osteosarcoma through activation of the VWF-GPIb axis
1Jiangsu Institute of Hematology, Key Laboratory of Thrombosis & Hemostasis of Ministry of Health, The First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Abstract:
von Willebrand factor (VWF) is exclusively expressed in endothelial cells (ECs) and megakaryocytes, which plays a crucial role in the initiation of arterial thrombosis. Recent studies have shown that VWF is also expressed in osteosarcoma (OS) cells and participates in adhesion of cancer cells to platelets, thus promoting metastasis of OS cells. However, it is unclear how OS cell-derived VWF-platelet interaction contributes to the metastasis of OS. We hypothesized that the interaction is mediated by the binding between VWF A1 and GPIbα of platelets, a molecular mechanism similar to that of thrombosis. The increased expression of VWF in SAOS2 cells may contribute to the enhancement of platelet adhesion through the VWF-GPIb pathway, which could promote the migration and invasion capacities of SAOS2 cells in vitro. Antibodies that block the pathway could significantly inhibit the platelet-induced metastasis of OS cells. Our results suggest a theoretical basis for the development of new anti-OS metastasis drugs, and further enrich the mechanism of OS metastasis.
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