ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2022
Loss of aryl hydrocarbon receptor suppresses the response of colonic epithelial cells to IL22 signaling by upregulating SOCS3.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2022. 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, 22 citations in OpenAlex.
- Article
- The multifaceted role of SOCS3 in colorectal cancer: molecular mechanisms and clinical implications.Molecular biology reports · 2026Review
- New insight into the role of SOCS family in immune regulation and autoimmune pathogenesis.Journal of advanced research · 2026Review
- An overview of the role of the gut microbiota in rheumatoid arthritis.Microbiome research reports · 2026Review
- Context-dependent functions of the aryl hydrocarbon receptor in gastrointestinal cancers: from microenvironmental regulation to precision targeted therapy.Frontiers in cell and developmental biology · 2026Review
- Decoding the gut-adipose-ovary axis in polycystic ovary syndrome: from metabolic dysregulation to oncological risk modulation.Frontiers in microbiology · 2026Review
- Morphological and transcriptional insights into the role of histone phosphorylation-related genes in early development of the chicken duodenum.Animal bioscience · 2025Article
- SOCS3: An Immunological Biomarker Offering Potential Therapeutic Targets for Malignant Tumors.Biological procedures online · 2025Review
- CRISPR screens and quantitative proteomics reveal remodeling of the aryl hydrocarbon receptor-driven proteome through PARP7 activity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cancer organoids: A platform in basic and translational research.Genes & diseases · 2024Review
- IL-38 regulates intestinal stem cell homeostasis by inducing WNT signaling and beneficial IL-1β secretion.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Tumor-Suppressive Functions of the Aryl Hydrocarbon Receptor (AhR) and AhR as a Therapeutic Target in Cancer.Biology · 2023Review
- Aryl Hydrocarbon Receptor (AhR) Signaling in Colonic Cells and Tumors.Receptors (Basel, Switzerland) · 2023Article
- Health Benefits of Coffee Consumption for Cancer and Other Diseases and Mechanisms of Action.International journal of molecular sciences · 2023Review
- Activation of the aryl hydrocarbon receptor in inflammatory bowel disease: insights from gut microbiota.Frontiers in cellular and infection microbiology · 2023Review
- Polyphenols as Drivers of a Homeostatic Gut Microecology and Immuno-Metabolic Traits ofInternational journal of molecular sciences · 2022Review
- Diabetes downregulates the antimicrobial peptide psoriasin and increases E. coli burden in the urinary bladder.Nature communications · 2022Article
- Human Adult Microbiota in a Static Colon Model: AhR Transcriptional Activity at the Crossroads of Host-Microbe Interaction.Foods (Basel, Switzerland) · 2022Article
- Revolutionizing digestive system tumor organoids research: Exploring the potential of tumor organoids.Journal of tissue engineeringReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
IL22 signaling plays an important role in maintaining gastrointestinal epithelial barrier function, cell proliferation, and protection of intestinal stem cells from genotoxicants. Emerging studies indicate that the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, promotes production of IL22 in gut immune cells. However, it remains to be determined if AhR signaling can also affect the responsiveness of colonic epithelial cells to IL22. Here, we show that IL22 treatment induces the phosphorylation of STAT3, inhibits colonic organoid growth, and promotes colonic cell proliferation in vivo. Notably, intestinal cell-specific AhR knockout (KO) reduces responsiveness to IL22 and compromises DNA damage response after exposure to carcinogen, in part due to the enhancement of suppressor of cytokine signaling 3 (SOCS3) expression. Deletion of SOCS3 increases levels of pSTAT3 in AhR KO organoids, and phenocopies the effects of IL22 treatment on wild-type (WT) organoid growth. In addition, pSTAT3 levels are inversely associated with increased azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colon tumorigenesis in AhR KO mice. These findings indicate that AhR function is required for optimal IL22 signaling in colonic epithelial cells and provide rationale for targeting AhR as a means of reducing colon cancer risk.
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Registered trials
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.