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78 reviewsSUMMARYBone marrow is both a primary site for hematopoiesis and a fertile niche for metastasis. The mechanism of thecommon occurrence of anemia among patients with bone metastasis remains poorly understood. Here, weshow that a specialized population of VCAM1+CD163+CCR3+ macrophages, normally essential for erythropoiesis by transporting iron to erythroblasts, are highly enriched in the bone metastatic niche in mousemodels. Tumor cells hijack these macrophages for iron supply, reducing iron availability for erythroblasts,impairing erythropoiesis, and contributing to anemia. Increased iron supply enables tumor cells to producehemoglobin in response to hypoxia, mimicking erythroblasts. We identify macrophages with similar irontransporting features in human bone metastases and show that elevated HBB expression correlates withincreased risk of bone metastasis. These findings establish iron-transporting macrophages as an essentialcomponent of the metastatic bone niche, revealing a critical interplay between immune cells, metalmetabolism, and tumor cell plasticity in driving metastasis and anemia.
