Abstract
Platelet activation is the first response to tissue damage and, if unrestrained, may promote chronic inflammation-related cancer, mainly through the release of soluble factors and vesicles that are rich in genetic materials and proteins. Platelets also sustain cancer cell invasion and metastasis formation by fostering the development of the epithelial-mesenchymal transition phenotype, cancer cell survival in the bloodstream and arrest/extravasation at the endothelium. Furthermore, platelets contribute to tumor escape from immune elimination. These findings provide the rationale for the use of antithrombotic agents in the prevention of cancer development and the reduction of metastatic spread and mortality. Among them, low-dose aspirin has been extensively evaluated in both preclinical and clinical studies. The lines of evidence have been considered appropriate to recommend the use of low-dose aspirin for primary prevention of cardiovascular disease and colorectal cancer by the USA. Preventive Services Task Force. However, two questions are still open: (i) the efficacy of aspirin as an anticancer agent shared by other antiplatelet agents, such as clopidogrel; (ii) the beneficial effect of aspirin improved at higher doses or by the co-administration of clopidogrel. This review discusses the latest updates regarding the mechanisms by which platelets promote cancer and the efficacy of antiplatelet agents.
Highlights
Antithrombotic agents mainly comprise two classes of drugs that are commonly used in clinical practice to combat pathologic thrombosis: antiplatelet drugs and anticoagulants
Numerous mechanistic studies have been performed in vitro and in vivo using animal models, and the results show that low-dose aspirin prevents metastasis development by interrupting the crosstalk between platelets and cancer cells [27,29]
These findings suggest a role for P2Y12 -R in mediating platelet–cancer cell crosstalk and provide evidence for the use of P2Y12 -R antagonists as an additional strategy in chemotherapy, no results from RCTs aimed at assessing their effect on cancer and metastasis are available
Summary
Antithrombotic agents mainly comprise two classes of drugs that are commonly used in clinical practice to combat pathologic thrombosis: antiplatelet drugs and anticoagulants. They share the common action of preventing a clot from forming and growing, but it is accomplished via different mechanisms [1]. Xa inhibitor fondaparinux) may affect the platelet release of angiogenic proteins through the inhibition of thrombin-dependent protease-activated receptor (PAR1) activation [5] This mechanism might play a role in the anticancer effects of UFH and LMWH, independent of their anticoagulant functions, found in preclinical studies [6]. This review discusses the latest updates regarding the mechanisms by which platelets promote cancer and the efficacy of antiplatelet agents
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