The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Figure 5

A schematic figure on the development of selectin-mediated heterotypic interactions among tumor cells, leukocytes, platelets, and endothelial cells during metastasis formation. Tumor cells circulate in the blood stream until they tether (I), roll (II), and then are arrested on endothelial cells (III) and finally migrate from the vasculature (IV). Activated platelets aggregate with cancer cells via P-selectin protecting them from innate immune system and permitting further leukocyte binding. Induced endothelial cell activation by tumor cells results in E- and P-selectin expression with additional recruitment of reactive neutrophils and monocytes to cancer cells regulated via L-selectin. As being magnified, selectin ligands (e.g., PSGL-1, sialyl-) are expressed on malignant cells to bind selectins that are expressed on normal blood cells and endothelial cells. See details in the text. Of note, there are several other receptors and integrins involved in these interactions but that cannot be depicted here.