Understanding the role of Oncostatin M signalling in the remodelling of the breast cancer immune microenvironment

Chronic inflammation is considered one of the main drivers of cancer progression and cytokines are key regulators of this inflammation. Recent data from our group support that cytokine Oncostatin M (OSM) acts as a key player in the interactions in the breast tumour microenvironment, where OSM activates an intriguing pro-tumoral signalling in cancer-associated fibroblasts (CAFs) and cancer cells. Our recent unpublished work characterised the effects of OSM in immune remodelling and immune suppression. Data from our laboratory supports the idea that OSM, mainly produced by myeloid cells, has a potential immunosuppressive effect by increasing macrophage and neutrophil recruitment and favoring the secretion of cytokines related to protumoral inflammation. Our next steps are focused on investigating which are the specific mechanisms by which OSM-OSMR axis changes immune cell populations and their phenotype in the tumor microenvironment and decipher if this axis could be a promising target for the development of new cancer immunotherapies.