血小板在血栓形成和止血中的作用已得到广泛认可。然而，血小板还通过与肿瘤微环境（TME）中的各种细胞进行相互作用来促进肿瘤的进展和转移。例如，多个癌症模型继续显示，癌细胞激活后能够改变血小板功能，导致形成血小板-肿瘤聚集物，触发血小板颗粒释放可溶性因子，并改变血小板的周转。此外，活化的血小板能够保护肿瘤细胞免受循环中的剪切力和细胞毒性自然杀伤（NK）细胞的攻击。血小板释放的因子促进恶性细胞增殖、转移和化疗耐药性。我们关于血小板在癌症中的生物学知识大部分是通过动物模型，尤其是小鼠模型，获得的。然而，这种临床前对复杂病理生理学的理解在通过控制血小板功能来治疗癌症的新方法方面尚未完全实现和转化为临床试验。在本综述中，我们总结了通过现有的体内和体外癌症模型获得的有关血小板生理学的当前研究进展，血小板与肿瘤细胞在TME中的复杂相互作用以及血小板可能赋予的化疗耐药性机制。由于美国政府最近通过的FDA现代化法案使动物模型在药物批准中成为可选择的，我们批判性地探讨了利用生物工程微物理系统和器官芯片来了解血小板在癌转移中的机制作用以及探索癌症预防和治疗的新靶点的现有和未来价值。

The contribution of platelets is well recognized in thrombosis and hemostasis. However, platelets also promote tumor progression and metastasis through their crosstalk with various cells of the tumor microenvironment (TME). For example, several cancer models continue to show that platelet functions are readily altered by cancer cells upon activation leading to the formation of platelet-tumor aggregates, triggering release of soluble factors from platelet granules and altering platelet turnover. Further, activated platelets protect tumor cells from shear forces in circulation and assault of cytotoxic natural killer (NK) cells. Platelet-secreted factors promote proliferation of malignant cells, metastasis, and chemoresistance. Much of our knowledge of platelet biology in cancer has been achieved with animal models, particularly murine. However, this preclinical understanding of the complex pathophysiology is yet to be fully realized and translated to clinical trials in terms of new approaches to treat cancer via controlling the platelet function. In this review, we summarize the current state of knowledge of platelet physiology obtained through existing in vivo and in vitro cancer models, the complex interactions of platelets with cancer cells in TME and the pathways by which platelets may confer chemoresistance. Since the FDA Modernization Act recently passed by the US government has made animal models optional in drug approvals, we critically examine the existing and futuristic value of employing bioengineered microphysiological systems and organ-chips to understand the mechanistic role of platelets in cancer metastasis and exploring novel therapeutic targets for cancer prevention and treatment.