CONICET | Buscador de Institutos y Recursos Humanos

Background/Aims: Some observations in experimental models had suggested that VWF can modulate the tumoral metastatic potential. The aim of this study was to explore whether human VWF affects the cell adhesion and viability of human (MCF-7) and mouse (F3II) breast and pulmonary (B16-F0) tumor cells. Materials and methods: Haemate-P (H) and sonicated H (SH; 20% amplitude, 3 minutes), were evaluated for VWF:Ag (10 IUmL-1, 8.6 IUmL-1, respectively) and VWF:CB (9.7 IUmL-1, 1.4 IUmL-1, respectively). Cells were incubated with H*; SH*; and vehicle (*VWF 0.5, 1 and 3 IUmL-1). Cellular proliferation was assessed using a colorimetric nonradioactive proliferation assay (MTS), and cell adhesion assay was evaluated by cell counts with Trypan Blue exclusion. GPIb mRNA was evaluated by RT-PCR and automated sequencing. VWF-binding to tumor cells was analyzed by flow cytometry (FC, median fluorescence intensity- MFI) and Cell-ELISA. Results: H induced cell death in a dose-dependent manner in F3II (10-30% cell death) and B16-F0 (10-20% cell death) cell lines. SH increased 1.2 to 1.5 folds the cell death regard to H. When cells were seeded in presence of H, MCF-7 and F3II were unable to adhere, while B16-F0 adhered to H in a dose-dependent manner (1.8 to 2.2 fold increase). MCF-7, F3II and B16-F0 expressed GPIb mRNA. After H treatment (1 IUmL-1), MCF-7 and F3II revealed VWF bound (positive control MFI= 19; MFI= 13), but B16-F0 (MFI= 1.2) did not; Cell-ELISA results confirmed these findings. Conclusions: Although all cell lines expressed GP1b, only F3II and MCF-7 showed VWF-binding but the last one failed in the cell death test in presence of H. VWF, regardless of function (H vs. SH), seems to be involved in the F3II cell line responses.