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Fig. 1 | Journal of Hematology & Oncology

Fig. 1

From: Role of platelets and platelet receptors in cancer metastasis

Fig. 1

Schematic overview of the metastatic cascade with focus on platelets. Tumor cells detach from the primary tumor and invade the blood circulation. Tumor cells immediately activate and are encased by platelets. Platelets secrete a plethora of growth factors and chemokines (like VEGF, PDGF, or TGF-β) upon activation which induce NK cell anergy due to NKG2D downregulation. In addition, granulocytes are attracted to the agglomerate of platelets and tumor cells by chemokines CXCL5 and CXCL7. Furthermore, platelets are capable to shift tumor cell phenotype from an epithelial to a mesenchymal-like. Finally, platelets mediate tumor cell arrest at the vascular wall via P-selectin and its ligands and facilitate tumor cell extravasation to the subendothelial matrix of a distant organ by activation of endothelial P2Y2 receptor. In order to establish a metastatic foci, platelet-derived growth factors, e.g., TGF-β, VEGF, or bFGF instigate tumor cell proliferation and neovessel formation

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