ArticleScientific reports2025
N6-methyladenosine (m6A)-forming enzyme METTL3 controls UAF1 stability to promote inflammation in a model of colitis by stimulating NLRP3.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- miR-192-5p targets USP1 to regulate osteogenic differentiation and diagnose the occurrence of osteoporotic fracture.BMC musculoskeletal disorders · 2026Article
- Mechanistic Networks, Cellular Specificity, and Therapeutic Opportunities of Ferroptosis in Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Review
- METTL3/YTHDF1 drives M1 macrophage polarization and aggravates ulcerative colitis progression by regulating m6A modification of SerpinB5 mRNA and FBXO32-dependent NF-κB pathway.Journal of gastroenterology · 2026Article
- Epitranscriptomic regulation by m6A in immunity and autoimmune disorders: emerging mechanisms and clinical perspectives.Frontiers in immunology · 2026Review
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5 authors.
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Abstract
backgroundThe rising incidence of ulcerative colitis (UC) in China poses a noticeable health challenge. This study aimed to assess the pivotal role of USP1-associated factor 1 (UAF1) in colitis. UC was induced in male C57BL/6 mice using 2.0% dextran sulfate sodium (DSS). In an in vitro model, RAW264.7 cells were exposed to 200 ng/ml of LPS + ATP. UAF1 expression level was evaluated in colonic tissues, macrophages, and serum samples using quantitative reverse transcription polymerase chain reaction (RT-qPCR). The study assessed weight, disease activity index (DAI) score, myeloperoxidase (MPO) activity, crypt length, inflammatory factors, and epithelial cell function in a mouse model of colitis treated with a UAF1 inhibitor. Microarray analysis identified potential UAF1 targets. Gene interference investigated NLR family pyrin domain containing 3 (NLRP3) involvement in UAF1-induced colitis inflammation. Immunoprecipitation, ubiquitination, and luciferase assays examined the effects of methyltransferase-like 3 (METTL3) methylation on the expression levels of NLRP3 and UAF1. UAF1 expression level was upregulated in colon tissues, RAW264.7 macrophages, and serum samples of colitis mice (P < 0.01). The UAF1 inhibitor (ML-323) enhanced weight and reduced DAI score in colitis mice (P < 0.01). It also decreased MPO activity and ulcer area, and restored crypt length (P < 0.01). UAF1 inhibitor improved epithelial cell function by suppressing NLRP3 activity (P < 0.01). UAF1 promoted inflammation in RAW264.7 macrophages via NLRP3 inflammasome induction (P < 0.01). UAF1 modulated NLRP3 protein expression, leading to reduced NLRP3 ubiquitination induced by LPS + ATP. The m6A-forming enzyme METTL3 enhanced UAF1 stability (P < 0.01) to facilitate UAF1 expression. The findings suggested that METTL3, as an m6A-forming enzyme, could regulate UAF1 mRNA, promoting inflammation in colitis through NLRP3 induction. Inhibiting UAF1 emerges as a potential therapeutic strategy for colitis.
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