| First Author | Kesselring R | Year | 2016 |
| Journal | Cancer Cell | Volume | 29 |
| Issue | 5 | Pages | 684-696 |
| PubMed ID | 27150039 | Mgi Jnum | J:231897 |
| Mgi Id | MGI:5775479 | Doi | 10.1016/j.ccell.2016.03.014 |
| Citation | Kesselring R, et al. (2016) IRAK-M Expression in Tumor Cells Supports Colorectal Cancer Progression through Reduction of Antimicrobial Defense and Stabilization of STAT3. Cancer Cell 29(5):684-96 |
| abstractText | 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. |
