What is it about?
We used MIF-knockout (MIF-/-) and wild-type (WT) mice to develop CRC. Greater tumor burdens were observed in MIF-/- mice than in WT mice. Tumors from MIF-/- mice were histologically identified to be more aggressive than tumors from WT mice. The localization of MIF suggests that it is also involved in cell differentiation. The expression of il-17 was higher in MIF-/- CRC mice, compared to the WT CRC. Importantly, compared to the WT intestinal epithelium, lower percentages of tumor-associated Møs were found in the MIF-/- intestinal epithelium. These results suggest that MIF plays a role in controlling the initial development of CRC.
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Why is it important?
This paper suggest that MIF plays a role in controlling the initial development of CRC by attracting Møs to the tumor, which is a condition that favors the initial antitumor responses. However, increased abnormal production of MIF by the tumor cells can be used as a proliferative advantage at later tumor stages.These observations are important for making decisions in treatments against colon cancer.
Perspectives
In MIF knockout mice, the lack of this “beneficial”-inflammation starter may favor the inflammatory Th17 pathway, but there is needed of further analysis to test this hypothesis.
Miriam Rodriguez-Sosa
Universidad Nacional Autonoma de Mexico
Read the Original
This page is a summary of: Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer, Mediators of Inflammation, July 2019, Hindawi Publishing Corporation,
DOI: 10.1155/2019/2056085.
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