Rab Safia Obaidur, Altalbawy Farag M A, Bishoyi Ashok Kumar, Ballal Suhas, Kareem Muthena, Singh Abhayveer, Kubaev Aziz, Soleimani Samarkhazan Hamed, Bagheri Saeede
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
Department of Chemistry, University College of Duba, University of Tabuk, Tabuk, Saudi Arabia.
Med Oncol. 2025 Jun 2;42(7):232. doi: 10.1007/s12032-025-02787-1.
Metastasis-the dissemination of cancer cells to distant organs-is the leading cause of cancer-related death. Beyond hemostasis, platelets contribute to tumor growth, angiogenesis, and metastasis by secreting factors such as platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β). These mediators stimulate tumor cell proliferation, migration, and invasion, fostering a microenvironment that promotes cancer progression. These factors stimulate the proliferation, migration, and invasion of tumor cells, contributing to the formation of a supportive tumor microenvironment that promotes cancer progression. On the other hand, tumor cells interact with platelets through various mechanisms, including the release of procoagulant factors, the expression of adhesion molecules, and induction of platelet activation and aggregation. This interaction forms a protective shield around circulating tumor cells, facilitating their escape from immune surveillance and promoting their infiltration into more distant sites. Platelets also play a significant role in modulating the tumor microenvironment. They contribute to immune suppression by inhibiting T-cell function, promoting the activity of immunosuppressive cells (e.g., myeloid-derived suppressor cells), and protecting tumor cells from immune attack. Understanding the complex interactions between platelets, tumor cells, and targeting platelet-tumor interactions (e.g., inhibiting platelet activation or PDGF signaling) may provide promising strategies. This review synthesizes recent advancements in understanding platelet-tumor crosstalk, with a focus on novel mechanisms such as platelet-derived microparticle-mediated metastasis, immune checkpoint mimicry by tumor-educated platelets, and the paradoxical roles of thrombospondin-1 (TSP-1) in angiogenesis. We critically evaluate emerging therapeutic strategies targeting platelet-tumor signaling and identify unresolved questions, including the role of platelet miRNAs in pre-metastatic niche formation and the efficacy of combinatorial antiplatelet-immunotherapy approaches.
转移——癌细胞扩散至远处器官——是癌症相关死亡的主要原因。除止血作用外，血小板通过分泌血小板衍生生长因子（PDGF）、血管内皮生长因子（VEGF）和转化生长因子-β（TGF-β）等因子，促进肿瘤生长、血管生成和转移。这些介质刺激肿瘤细胞增殖、迁移和侵袭，营造促进癌症进展的微环境。这些因子刺激肿瘤细胞的增殖、迁移和侵袭，有助于形成促进癌症进展的支持性肿瘤微环境。另一方面，肿瘤细胞通过多种机制与血小板相互作用，包括释放促凝血因子、表达黏附分子以及诱导血小板活化和聚集。这种相互作用在循环肿瘤细胞周围形成一个保护屏障，便于其逃避免疫监视并促进其浸润至更远的部位。血小板在调节肿瘤微环境方面也发挥着重要作用。它们通过抑制T细胞功能、促进免疫抑制细胞（如骨髓来源的抑制细胞）的活性以及保护肿瘤细胞免受免疫攻击来促成免疫抑制。了解血小板与肿瘤细胞之间的复杂相互作用以及靶向血小板-肿瘤相互作用（如抑制血小板活化或PDGF信号传导）可能会提供有前景的策略。本综述综合了在理解血小板-肿瘤串扰方面的最新进展，重点关注诸如血小板衍生微粒介导的转移、肿瘤驯化血小板的免疫检查点模拟以及血小板反应蛋白-1（TSP-1）在血管生成中的矛盾作用等新机制。我们批判性地评估了针对血小板-肿瘤信号传导的新兴治疗策略，并确定了尚未解决的问题，包括血小板微小RNA在转移前生态位形成中的作用以及联合抗血小板免疫治疗方法的疗效。
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