Cancer metastasis is a unique feature of malignant tumours. Even bone can become a common colonization site due to the tendency of solid tumours, including breast cancer (BCa) and prostate cancer (PCa), to metastasize to bone. Currently, a previous concept in tumour metabolism called tumour dormancy may be a promising target for antitumour treatment. When disseminated tumour cells (DTCs) metastasize to the bone microenvironment, they form a flexible regulatory network called the “bone-tumour-inflammation network”. In this network, bone turnover as well as metabolism, tumour progression, angiogenesis and inflammatory responses are highly unified and coordinated, and a slight shift in this balance can result in the disruption of the microenvironment, uncontrolled inflammatory responses and excessive tumour growth. The purpose of this review is to highlight the regulatory effect of the “bone-tumour-inflammation network” in tumour dormancy. Osteoblast-secreted factors, bone turnover and macrophages are emphasized and occupy in the main part of the review. In addition, the prospective clinical application of tumour dormancy is also discussed, which shows the direction of future research.

癌症转移是恶性肿瘤的一个独特特征。由于包括乳腺癌 (BCa) 和前列腺癌 (PCa) 在内的实体瘤倾向于转移到骨骼，因此甚至骨骼也可能成为常见的定植部位。目前，肿瘤代谢中的一个先前概念称为肿瘤休眠，可能是抗肿瘤治疗的一个有希望的目标。当播散性肿瘤细胞（DTC）转移到骨微环境时，它们形成一个灵活的调节网络，称为“骨肿瘤炎症网络”。在这个网络中，骨转换以及新陈代谢、肿瘤进展、血管生成和炎症反应是高度统一和协调的，这种平衡的轻微改变就会导致微环境的破坏、炎症反应失控和肿瘤过度生长。本综述的目的是强调“骨-肿瘤-炎症网络”在肿瘤休眠中的调节作用。成骨细胞分泌因子、骨转换和巨噬细胞被强调并占据了综述的主要部分。此外，还讨论了肿瘤休眠的前瞻性临床应用，指明了未来研究的方向。