Abstract
Platelets contribute to several types of cancer through plenty of mechanisms. Upon activation, platelets release many molecules, including growth and angiogenic factors, lipids, and extracellular vesicles, and activate numerous cell types, including vascular and immune cells, fibroblasts, and cancer cells. Hence, platelets are a crucial component of cell–cell communication. In particular, their interaction with cancer cells can enhance their malignancy and facilitate the invasion and colonization of distant organs. These findings suggest the use of antiplatelet agents to restrain cancer development and progression. Another peculiarity of platelets is their capability to uptake proteins and transcripts from the circulation. Thus, cancer-patient platelets show specific proteomic and transcriptomic expression patterns, a phenomenon called tumor-educated platelets (TEP). The transcriptomic/proteomic profile of platelets can provide information for the early detection of cancer and disease monitoring. Platelet ability to interact with tumor cells and transfer their molecular cargo has been exploited to design platelet-mediated drug delivery systems to enhance the efficacy and reduce toxicity often associated with traditional chemotherapy. Platelets are extraordinary cells with many functions whose exploitation will improve cancer diagnosis and treatment.
Highlights
Platelets are known for their role in hemostasis and thrombosis [1,2]
All these lines of evidence support the pivotal role of platelets in promoting early cancerogenic signaling pathways restrained by aspirin [8,15,16]
The known determinants of the interactions between platelets and cancer cells are reported with possible inhibitory pharmacological tools that have been described. These findings suggest that selecting a specific pharmacological agent to constrain metastasis development requires the characterization of the altered expression of tumor molecules involved in the interaction with platelets
Summary
Platelets are known for their role in hemostasis and thrombosis [1,2]. They are anucleated cells arising from cytoplasmic fragmentation of megakaryocytes, mainly in the bone marrow, and contain various mediators stored in at least three major types of granules—α-granules, dense granules, and lysosomes. Single dosing of 400 mg of celecoxib significantly reduced average urinary PGI-M levels by 70–80%, which was not significantly different from the inhibitory effect of the nonselective nonsteroidal anti-inflammatory drugs (NSAID) ibuprofen (800 mg) [20] These results suggest a dominant contribution of COX-2 to the systemic biosynthesis of prostacyclin [22]. A 75 mg controlled-release preparation of aspirin with low bioavailability, which inhibits platelet COX-1 in the presystemic circulation associated with marginal systemic effects [36], was used in the Thrombosis Prevention Trial (TPT) for the primary prevention of cardiovascular disease [37] This trial was included in Rothwell’s analysis of five large randomized trials of daily aspirin (≥75 mg daily) versus control [33]. Loaded platelets with an anticancer agent administered to mouse models of cancer deliver the compound to malignant cells via the release of vesicles containing it [41]
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