The role of platelets in tumor immune evasion and metastasis: mechanisms and therapeutic implications.

Abstract

Only circulating tumor cells (CTCs) that successfully evade immune surveillance upon entering the bloodstream can lead to clonal expansion and metastasis. Cancer progression is accompanied by pathophysiological processes such as platelet activation and thrombosis. Platelets secrete a variety of growth factors to stimulate cancer cell proliferation, regulate tumor angiogenesis, and subsequently mediate surface changes in cancer cells to promote invasion and progression. As part of a dangerous alliance, CTCs and platelets induce mutual activation. Activated platelets aggregate and encapsulate tumor cells, forming microtumor thrombi containing fibrin clots that act as protective barriers. These platelets interact with immune cells, including NK cells, macrophages, neutrophils, and T cells, to facilitate cancer metastasis and progression through various mechanisms. The formation of a favorable tumor microenvironment (TME) and pre-metastatic niche aids cancer cells in evading immune surveillance. Multiple signaling pathways and immune checkpoints are also involved in this process. Given the significant role of platelets in tumor immune evasion, anti-cancer strategies targeting platelets and their potential use as "bionic drug delivery systems" for anti-tumor drugs hold broad prospects in emerging tumor therapies.