Inflammation joins the "niche"

Abstract

Bone marrow-derived cells have an important role in tumor metastasis and have been reported to "prime" distant tissues for tumor engraftment, although the mechanisms for their recruitment have remained unclear. A new study by Hiratsuka et al. describes an inflammatory signaling pathway that mediates the chemoattraction of myeloid and tumor cells to organ-specific metastatic sites.

Figure 1. The Premetastatic Niche Is Similar to an Inflammatory Nidus

Both S100A8 and S100A9 induce the expression of SAA3 specifically in future metastasis sites in the lung, promoting Mac1⁺ myeloid and endothelial cell engraftment. In this process, SAA3 promotes its own secretion by a positive feedback mechanism mediated by TLR4 and induces NF-κB signaling pathway activation (left). This inflammation-like state accelerates the future recruitment of tumor cells (right).