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. 2021 Oct 14;11:764119. doi: 10.3389/fonc.2021.764119

Figure 1.

Figure 1

The bidirectional interaction between cancer cells and platelets. Cancer cells promote platelet production and activation, while activated platelets release a number of mediators to facilitate tumor growth and cancer cell metastasis. Activated platelets prevent circulating cancer cells (CTCs) from shear flow, immune surveillance and apoptosis, thus enhancing CTC survival in circulation. They also facilitate CTC adhesion, angiogenesis and invasion thereby enhancing metastasis. IL-1β, Interleukin-1β; IL-6, Interleukin-6; TPO, thrombopoietin; G-CSF, Granulocyte- Colony-Stimulating Factor; GM-CSF, Granulocyte-Macrophage-Colony-Stimulating Factor; TF, Tissue Factor; HGMB1, High-Mobility Group Box1; TXA2, Thromboxane A2; IgG, immunoglobulin G; PDPN, Podoplanin; CLEC2, C-type lectin receptor type 2; NETs, Neutrophil Extracellular Traps; TGFβ, Transforming Growth Factor β; PDGF, Platelet-Derived Growth Factor; VEGF, Vascular Endothelial Growth Factor; PF4, Platelet Factor 4; TCIPA, Tumor Cell-Induced Platelet Aggregation; MHC I, MHC class I; ADAM10, Disintegrin And Metalloproteinase Domain-Containing Protein 10; GITRL, Glucocorticoid-Induced TNF Receptor-Related Ligand; RANKL, Receptor Activator of NF-κB Ligand; OX40L, Oxford 40 Ligand; GARP, Glycoprotein A Repetitions Predominant; PD-L1, Programmed Cell Death-Ligand 1; PMPs, Platelet Microparticles; PECAM-1, Platelet-Endothelial Cell Adhesion Molecule-1; PSGL-1, P-selectin Glycoprotein Ligand-1.