Background: It is well known that platelets support cancer cells in nearly every step of metastasis [1]. During tumor cell-induced platelet-activation platelets release a plethora of mediators, platelet-derived microparticles (PMPs) and exosomes that regulate cancer cell activities. Furthermore, activated platelets bind to cancer cells and form a platelet cloak around cancer cells as a physical barrier to protect the cancer cell from immune surveillance and facilitate cancer cells sustained adhesion to the vessel wall, extravasation and metastasis. Among these different ways platelets unfold their protumorigenic and prometastatic effect another way of transfer between platelets and cancer cells remained almost unnoticed: The phagocytic uptake of platelets. Methods: We used human non-small cell lung cancer cells (A549) and freshly isolated human platelets to study their interaction in suspension. A549 cells were incubated for different time intervals with fluorescently labelled platelets on a tilting table and under laminar flow conditions. Samples were analysed by confocal laser scanning microscopy (CLSM) and fluorescence-based flow cytometry (FACS). Results: Current research indicates a cloak-formation of platelets around circulating cancer cells. We never observed such cloak formation, instead, all experiments showed an uptake of platelets by A549 cells. The half-maximal uptake was observed after 38 min. This platelet uptake was completely abolished by the Dynamin inhibitor Dyngo4a. This, together with CLSM images indicate a phagocytic uptake of platelets by A549 cancer cells. Immunofluorescence staining of the platelet specific proteins CD42a (GP IX) and GPIIb/IIIa after A549-platelet incubation revealed an appearance of these proteins in the plasma membrane of A549 cells. CLSM scans of the FACS samples proved that there was no platelet attached to A549 cells. Staining of platelets with a FITC-labeled anti-CD42a antibody prior to incubation and time-laps CLSM indicated an endosomal escape of CD42a. We performed platelet uptake experiments with another highly metastatic cell line, the melanoma derived MV3 cells and with the non-cancerous, SV40 large T-antigen transformed, lung epithelial cell line (16HBE14o-). Incubation with PKH67 stained platelets for 1h revealed an uptake of platelets in both cancerous cell lines but not in the immortalized cells. This preliminary data indicate that the uptake of platelets represents a more general mechanism by which cancer cells hijack the service of platelets Conclusion: Cancer cells phagocytose platelets to utilize platelet proteins through phagocytic recycling to their cell surface. This was shown for the cell adhesion proteins CD42a and GPIIb/IIIa. This novel insights in platelet-cancer cell interactions will allow further mechanistic elucidation of platelet-assisted metastasis and thus may contribute to the optimization of cancer therapies.