Tumor-mediated remote regulation of peripheral blood platelets

The role of platelets in blood coagulation and vascular repair is well known. In recent years, extensive attention has been given to the fact that the impact of tumors on peripheral blood platelets plays a key role in cancer progression. This review systematically summarizes the latest research progress on how tumors regulate the quantity, volume, composition, and activation status of peripheral blood platelets through multiple mechanisms. First, tumor cells can induce excessive platelet production by activating AhR-RUNX1 signaling through paracrine pathways and the release of kynurenine, thereby leading to thrombocytosis, which is associated with advanced tumor stages, metastasis, and poor prognosis. Second, tumor progression may trigger disseminated intravascular coagulation (DIC) or chemotherapy-related bone marrow suppression, which in turn results in consumptive thrombocytopenia. In addition, dynamic changes in the mean platelet volume (MPV) are related to tumor type and progression stage, which may reflect abnormal megakaryocyte differentiation or inflammatory status. In terms of platelet composition, tumor cells can remodel the proteome and transcriptome of platelets by secreting ADP, IgG, and functional RNA. Changes in RNA profiles have been confirmed to have potential for tumor diagnosis. In terms of activation status, tumor cells can induce platelet activation and aggregation (TCIPA) by releasing procoagulant factors such as tissue factors and exosomes (EVs), accelerating thrombosis and promoting angiogenesis. In clinical applications, platelet-related biomarkers have become a research hotspot for early cancer diagnosis and prognostic evaluation. Moreover, targeting platelets affected by tumors provides new strategies for tumor treatment. On the basis of the scientific findings of numerous existing studies, it is speculated that there seems to be a "dynamic balance" among platelets, which also provides a new direction for future research.