ArticleOncogene2021
Loss of interleukin-17 receptor D promotes chronic inflammation-associated tumorigenesis.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Role of microRNA-136 inWorld journal of gastrointestinal oncology · 2026Article
- Advances in molecular mechanisms of inflammatory bowel disease‑associated colorectal cancer (Review).Oncology letters · 2024Review
- Endothelial IL17RD promotes Western diet-induced aortic myeloid cell infiltration.Biochemical and biophysical research communications · 2024Article
- Tissue adaptation of CD4 T lymphocytes in homeostasis and cancer.Frontiers in immunology · 2024Article
- The role of interleukin-17 in inflammation-related cancers.Frontiers in immunology · 2024Review
- Exploring causal associations between interleukins, their receptors, and acute respiratory distress syndrome: a bidirectional-Mendelian Randomization study.Frontiers in genetics · 2024Article
- Article
- Molecular Mechanisms ofPharmaceutics · 2022Article
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- Single-cell atlas of the aging mouse colon.iScience · 2022Article
- TNFAIP8 protein functions as a tumor suppressor in inflammation-associated colorectal tumorigenesis.Cell death & disease · 2022Article
- Increased ten-eleven translocation methylcytosine dioxygenase one in dorsal root ganglion contributes to inflammatory pain in CFA rats.Molecular pain · 2022Article
- Review
- Soluble Endoglin Stimulates Inflammatory and Angiogenic Responses in Microglia That Are Associated with Endothelial Dysfunction.International journal of molecular sciences · 2022Article
- Respiratory immune status and microbiome in recovered COVID-19 patients revealed by metatranscriptomic analyses.Frontiers in cellular and infection microbiology · 2022Article
- Review
- Interleukin-17 Receptor D in Physiology, Inflammation and Cancer.Frontiers in oncology · 2021Review
- Nicotinamide Mononucleotide Alleviates Hyperosmolarity-Induced IL-17a Secretion and Macrophage Activation in Corneal Epithelial Cells/Macrophage Co-Culture System.Journal of inflammation research · 2021Article
- Several Fusion Genes Identified in a Spermatic Cord Leiomyoma With Rearrangements of Chromosome Arms 3p and 21q.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17 receptor D (IL-17RD), also known as similar expression to Fgf genes (SEF), is proposed to act as a signaling hub that negatively regulates mitogenic signaling pathways, like the ERK1/2 MAP kinase pathway, and innate immune signaling. The expression of IL-17RD is downregulated in certain solid tumors, which has led to the hypothesis that it may exert tumor suppressor functions. However, the role of IL-17RD in tumor biology remains to be studied in vivo. Here, we show that genetic disruption of Il17rd leads to the increased formation of spontaneous tumors in multiple tissues of aging mice. Loss of IL-17RD also promotes tumor development in a model of colitis-associated colorectal cancer, associated with an exacerbated inflammatory response. Colon tumors from IL-17RD-deficient mice are characterized by a strong enrichment in inflammation-related gene signatures, elevated expression of pro-inflammatory tumorigenic cytokines, such as IL-17A and IL-6, and increased STAT3 tyrosine phosphorylation. We further show that RNAi depletion of IL-17RD enhances Toll-like receptor and IL-17A signaling in colon adenocarcinoma cells. No change in the proliferation of normal or tumor intestinal epithelial cells was observed upon genetic inactivation of IL-17RD. Our findings establish IL-17RD as a tumor suppressor in mice and suggest that the protein exerts its function mainly by limiting the extent and duration of inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.