Kesselring, Rebecca and Glaesner, Joachim and Hiergeist, Andreas and Naschberger, Elisabeth and Neumann, Helmut and Brunner, Stefan M. and Wege, Anja K. and Seebauer, Caroline and Koehl, Gudrun and Merkl, Susanne and Croner, Roland S. and Hackl, Christina and Stuerzl, Michael and Neurath, Markus F. and Gessner, Andre and Schlitt, Hans-Juergen and Geissler, Edward K. and Fichtner-Feigl, Stefan (2016) IRAK-M Expression in Tumor Cells Supports Colorectal Cancer Progression through Reduction of Antimicrobial Defense and Stabilization of STAT3. CANCER CELL, 29 (5). pp. 684-696. ISSN 1535-6108, 1878-3686
Full text not available from this repository. (Request a copy)Abstract
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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | INTESTINAL INFLAMMATION; COLON-CANCER; KAPPA-B; COLITIS; ACTIVATION; RECEPTOR; TUMORIGENESIS; MICROBIOTA; HOMEOSTASIS; METASTASIS; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 20 Mar 2019 12:23 |
| Last Modified: | 20 Mar 2019 12:23 |
| URI: | https://pred.uni-regensburg.de/id/eprint/2941 |
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