The interactions between platelets and cancer cells play a crucial role in cancer metastasis, particularly within the dynamic environment of blood circulation, where the high abundance of blood cells inevitably influence these interactions. We employ a sophisticated numerical method, smoothed dissipative particle dynamics enhanced by GPU computations, to investigate the biomechanical interactions among platelets, cancer cells and red blood cells. Our simulations, spanning from molecular-level aggregation to cellular-level adhesion and further to the flow-level hemodynamics, provide a multiscale and multidimensional perspective on the biomechanical dynamics of cellular interactions during cancer metastasis. Our findings reveal that platelets play a dual role: those adhering to the vascular endothelium can capture tumor cells and facilitate their adhesion, while those circulating freely can aggregate tumor cells into heterogeneous clusters, exhibiting a secondary tethering phenomenon. Conversely, red blood cells act as physical barriers, disrupting cell aggregation and impeding the formation of secondary tethers, thus playing a protective role against metastasis. Furthermore, the variations in blood flow velocity and hematocrit levels is found to significantly affect the residence time of cancer cells within vessels, thereby influencing the likelihood of metastasis. 
 

Dissipative particle dynamics; Platelet; Cancer metastasis; Red blood cell