The absence of macrophages migration inhibitory factor (MIF) reduces the number of tumors in colitits.associated colorectal cancer

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Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B104
Abstract ID: 5670

Presenting Author:
Miriam Rodriguez-Sosa , The absence of MIF reduces the number of tumors in colitis-associated colorectal cancer at Univ. Nacional Autónoma de México, Univ. Nacional Autónoma de México Fac. de Estudios Superiores Iztacala

Abstract:

Background. Colorectal cancer (CRC) is ranking fourth in incidence and third in mortality among cancers in the world. The colitis inflammation associted is a main factor involved in CRC developement. Macrophages migration inhibitory factor (MIF) is a pro-inflammatory cytokine overexpressed in colitis, as in CRC. Objective. Here, we explored the role of endogenous MIF in the genesis and progression of CRC Methods. MIF gene-deficient (mif-/-) and wild-type (mif+/+) C57BL/6 mice were used to study the role for MIF in chemically CRC incuction (azoxymethane intraperitoneal injection -AOM-, 10 mg/Kg and 2% of dextran sodium sulphate -DSS-). After the induction clinical signs, and mortality were recorded weekly. Results. At 90 days post-induction, MIF enhanced the loss of goblet cells and subserved further cellular transformation which precedes adenoma development in CAC mice. MIF promoted number, size and tumoral burden and also triggers further clinical signs and symptoms in CAC mice. MIF increased DCs and M2 macrophages in the colon and CD8 lymphocytes in the spleen but decreased NK cells and MSDCs in the latter. Finally, MIF augmented the presence of M2 macrophages and NK cells but diminished M1 macrophages in the tumor. These findings suggest that MIF promotes inflammation by producing epithelial damage and cellular infiltration. Conclusion. MIF plays an important role regulating tumor maintenance in the CRC, highlighting MIF as a possible therapeutic target in CRC.