ArticleJCI insight2022
MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Systematic Review and Meta-analysis of Peripheral Blood DNA Methylation Studies in Inflammatory Bowel Disease.Journal of Crohn's & colitis · 2023Pooled it
- CBFA2T3 as a Key Prognostic Biomarker in Lung Adenocarcinoma: Insights from Comprehensive Analysis and Validation.Biochemical genetics · 2026Article
- Mtg16 NHR1 mutations cause defects in lymphopoiesis and the response to anemia.Experimental hematology · 2025Article
- Therapeutic targeting of the NOTCH1 and neddylation pathways in T cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- MTGR1 is required to maintain small intestinal stem cell populations.Cell death and differentiation · 2024Article
- CBFA2T3 Is PPARA Sensitive and Attenuates Fasting-Induced Lipid Accumulation in Mouse Liver.Cells · 2024Article
- Article
- Identification of cancer stemness and M2 macrophage-associated biomarkers in lung adenocarcinoma.Heliyon · 2023Article
- SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactions.The Journal of clinical investigation · 2023Article
- GWAS on Imputed Whole-Genome Sequence Variants Reveal Genes Associated with Resistance toGenes · 2022Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 4 countries.
Funding
Abstract
Aberrant epithelial differentiation and regeneration contribute to colon pathologies, including inflammatory bowel disease (IBD) and colitis-associated cancer (CAC). Myeloid translocation gene 16 (MTG16, also known as CBFA2T3) is a transcriptional corepressor expressed in the colonic epithelium. MTG16 deficiency in mice exacerbates colitis and increases tumor burden in CAC, though the underlying mechanisms remain unclear. Here, we identified MTG16 as a central mediator of epithelial differentiation, promoting goblet and restraining enteroendocrine cell development in homeostasis and enabling regeneration following dextran sulfate sodium-induced (DSS-induced) colitis. Transcriptomic analyses implicated increased Ephrussi box-binding transcription factor (E protein) activity in MTG16-deficient colon crypts. Using a mouse model with a point mutation that attenuates MTG16:E protein interactions (Mtg16P209T), we showed that MTG16 exerts control over colonic epithelial differentiation and regeneration by repressing E protein-mediated transcription. Mimicking murine colitis, MTG16 expression was increased in biopsies from patients with active IBD compared with unaffected controls. Finally, uncoupling MTG16:E protein interactions partially phenocopied the enhanced tumorigenicity of Mtg16-/- colon in the azoxymethane/DSS-induced model of CAC, indicating that MTG16 protects from tumorigenesis through additional mechanisms. Collectively, our results demonstrate that MTG16, via its repression of E protein targets, is a key regulator of cell fate decisions during colon homeostasis, colitis, and cancer.
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