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. 2015 Oct 20;5:224. doi: 10.3389/fonc.2015.00224

Figure 3.

Figure 3

Survival in the blood: ECM components as physical shields and mediators of platelet recruitment. In order to survive the high shear forces and patrolling NK-cells in the blood circulation, tumor cells interact with platelets. This association is mainly initiated by fibrinogen. Fibrinogen binding to tumor-expressed αvβ3 and platelet-derived integrin αIIbβ3 induces the formation of cancer-cell–fibrinogen–platelet complexes. In addition, tenascin C association with integrin α2β1 or the glycoprotein Ib-IX complex enhances platelet adhesion and activation. An HA-rich pericellular matrix further shields the cancer cells from NK-cell attack.