Journal
CANCER CELL
Volume 29, Issue 5, Pages 684-696Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2016.03.014
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Funding
- Deutsche Forschungsgemeinschaft [Fi1526/4-1, Fi1526/5-1, KFO 257 CEDER STU238/6-1]
- Regensburg Center of Interventional Immunology
- German Cancer Aid [109510]
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Colorectal cancer (CRC) is associated with loss of epithelial barrier integrity, which facilitates the interaction of the immunological microenvironment with the luminal microbiome, eliciting tumor-supportive inflammation. An important regulator of intestinal inflammatory responses is IRAK-M, a negative regulator of TLR signaling. Here we investigate the compartment-specific impact of IRAK-M on colorectal carcinogenesis using a mouse model. We demonstrate that IRAK-M is expressed in tumor cells due to combined TLR and Wnt activation. Tumor cell-intrinsic IRAK-M is responsible for regulation of microbial colonization of tumors and STAT3 protein stability in tumor cells, leading to tumor cell proliferation. IRAK-M expression in human CRCs is associated with poor prognosis. These results suggest that IRAK-M may be a potential therapeutic target for CRC treatment.
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