Chemokine Property Of MIF Favors Immunosurveillance In Murine Colorectal Cancer

Chronic inflammation has been related with cancer development by unbalancing immune response. The inflammatory cytokine macrophage migration inhibitory factor (MIF) is overexpressed in many carcinogenic tumors, stimulates angiogenesis and metastasis promoting proliferation and survival in malignant cells and binds to CD74 (ligand for CXCR2 and CXCR4). In  ulcerative colitis MIF is early expressed and favors the inflammatory cytokine production like TNF-α and IL-β. As intestinal chronic inflammation may precede colorectal cancer, we are interested in determining the role of MIF on pathology of colorectal cancer. We used MIF^-/- and WT mice to develop a colorectal cancer model of Dextran Sodium Sulfate and Azoxymethane. Strikingly, we found significantly more tumors and in higher development stage on MIF^-/- (24.4±2) compared to WT (12.6±2). Higher number of activated macrophages were found in WT mice intestinal epithelium compared to MIF^-/- mice. Therefore, although MIF has been recognized as a promoter of inflammation, which could favor cancer development; our results suggest that MIF is involved in important cells recruitment, like macrophages, to control colorectal cancer development, possibly by its chemokine property. Supported by CONACyT (152224), PAPCA-16 and PAPIIT IN212215.