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. 2017 Sep 28;9(10):133. doi: 10.3390/cancers9100133

Figure 1.

Figure 1

Physical and functional platelet–tumor cell crosstalk. Tumor metastasis is a complex process including the detachment of tumor cells from the primary tumor, intravasation, survival in the bloodstream, extravasation, and proliferation at the distant site. Following intravasation, tumor cells enter into the bloodstream and get in close contact with various circulating blood cells including platelets. Platelets physically interact with tumor cells through the binding of CLEC-2, P-selectin, and integrins α6β1 and αIIbβ3 with podoplanin, PSGL-1, ADAM-9 and fibrinogen/αvβ3, respectively. The role of platelet integrins α2β1, α5β1, and αvβ3 in direct interaction with tumor cells remains unknown. Platelet adhesion to tumor cells results in their activation, which promotes: (i) platelet shape change; (ii) integrin αIIbβ3 activation upon talin and kindlin binding to the intracytoplasmic domain of the β3 chain; (iii) the release of biologically active molecules including TxA2, ADP, ATP, MMP-2, TGF-β, and Vascular endothelial growth factor (VEGF). In turn, these mediators promote: (i) Tumor cell induced platelet aggregation (TCIPA); (ii) tumor cell invasion; (iii) EMT; and (iv) angiogenesis.