Platelet--cancer interactions: mechanisms and pharmacology of tumour cell-induced platelet aggregation

Abstract

During haematogenous metastasis, cancer cells migrate to the vasculature and interact with platelets resulting in tumour cell-induced platelet aggregation (TCIPA). We review: 1. The biological and clinical significance of TCIPA; 2. Molecular mechanisms involved in platelet aggregation by cancer cells; 3. Strategies for pharmacological regulation of these interactions. We conclude that pharmacological regulation of platelet-cancer cell interactions may reduce the impact of TCIPA on cancer biology.

Figure 1

Major mechanisms and pharmacology of TCIPA depicting the interactions between tumour cells, platelets, and endothelial cells. Mediators and antagonists of TCIPA are shown in blue and red, respectively. ASA, acetyl salicylic acid; COX-1, cyclooxygenase-1; GSNO, S-nitrosoglutathione, MMPIs, matrix metalloproteinase inhibitors; 2-MeSAMP, 2-methylthio-AMP; PGI₂, prostacyclin; SNAP, S-nitroso-N-acetylpenicillamine; TF, tissue factor, vWF, von Willebrand factor.