# name
Stromal Oncostatin M cytokine promotes breast cancer progression by reprogramming the tumour microenvironment

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The tumor microenvironment (TME) is reprogrammed by cancer cells and participates in all stages of tumor progression.  The contribution of stromal cells to the reprogramming of the TME is not well understood. Here, we provide evidence of the  role of the cytokine oncostatin M (OSM) as central node for multicellular interactions between immune and nonimmune  stromal cells and the epithelial cancer cell compartment. OSM receptor (OSMR) deletion in a multistage breast cancer model  halted tumor progression. We ascribed causality to the stromal function of the OSM axis by demonstrating reduced tumor  burden of syngeneic tumors implanted in mice lacking OSMR. Single-cell and bioinformatic analysis of murine and human  breast tumors revealed that OSM expression was restricted to myeloid cells, whereas OSMR was detected predominantly  in fibroblasts and, to a lower extent, cancer cells. Myeloid-derived OSM reprogrammed fibroblasts to a more contractile and  tumorigenic phenotype and elicited the secretion of VEGF and proinflammatory chemokines CXCL1 and CXCL16, leading to  increased myeloid cell recruitment. Collectively, our data support the notion that the stromal OSM/OSMR axis reprograms the  immune and nonimmune microenvironment and plays a key role in breast cancer progression.

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American Society for Clinical Investigation

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Journal of Clinical Investigation, 2022, vol. 132, num.19

# metadata.dc.rights[].value
(c) American Society for Clinical Investigation, 2022

# metadata.dc.source[].value
Articles publicats en revistes (Biomedicina)

# metadata.dc.title[].value
Stromal Oncostatin M cytokine promotes breast cancer progression by reprogramming the tumour microenvironment