ArticleOncotarget2017
MicroRNA-206 is involved in the pathogenesis of ulcerative colitis via regulation of adenosine A3 receptor.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Purinergic signaling in the gut neuro-glial-immune axis: mechanisms of homeostasis, inflammation, and gastrointestinal dysfunction.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Advances in biosensors for diagnosis and monitoring of inflammatory bowel disease: A review.Bioengineering & translational medicine · 2025Review
- MicroRNA-microbiota interactions: Emerging strategies for modulating intestinal homeostasis and enhancing host health.iMetaOmics · 2025Review
- METTL14 regulates inflammation in ulcerative colitis via the lncRNA DHRS4-AS1/miR-206/A3AR axis.Cell biology and toxicology · 2024Article
- MicroRNA signatures in the pathogenesis and therapy of inflammatory bowel disease.Clinical and experimental medicine · 2024Review
- miRNA-206-3p alleviates LPS-induced acute lung injury via inhibiting inflammation and pyroptosis through modulating TLR4/NF-κB/NLRP3 pathway.Scientific reports · 2024Article
- Long Non-Coding RNA ANRIL Regulates Inflammatory Factor Expression in Ulcerative Colitis Via the miR-191-5p/SATB1 Axis.Inflammation · 2024Article
- Adenosine-mediated immune responses in inflammatory bowel disease.Frontiers in cell and developmental biology · 2024Review
- MicroRNA: Crucial modulator in purinergic signalling involved diseases.Purinergic signalling · 2023Review
- Article
- miRNA effects on gut homeostasis: therapeutic implications for inflammatory bowel disease.Trends in immunology · 2022Review
- miRNAs Can Affect Intestinal Epithelial Barrier in Inflammatory Bowel Disease.Frontiers in immunology · 2022Review
- Targeting G protein-coupled receptors for the treatment of chronic pain in the digestive system.Gut · 2021Review
- miRNA-Based Potential Biomarkers and New Molecular Insights in Ulcerative Colitis.Frontiers in pharmacology · 2021Review
- Rab27A promotes cellular apoptosis and ROS production by regulating the miRNA-124-3p/STAT3/RelA signalling pathway in ulcerative colitis.Journal of cellular and molecular medicine · 2020Article
- The Adenosine System at the Crossroads of Intestinal Inflammation and Neoplasia.International journal of molecular sciences · 2020Review
- Upregulation of microRNA-219-5p relieves ulcerative colitis through balancing the differentiation of Treg/Th17 cells.European journal of gastroenterology & hepatology · 2020Article
- Inflammatory Bowel Diseases: It's Time for the Adenosine System.Frontiers in immunology · 2020Article
- The Purinergic System as a Pharmacological Target for the Treatment of Immune-Mediated Inflammatory Diseases.Pharmacological reviews · 2019Review
- AMedicinal research reviews · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that miRNAs are widely dysregulated in ulcerative colitis (UC), potentially affecting UC pathogenesis, diagnosis, and therapy. microRNA (miR) -206 has been reported to be upregulated in UC; however, its function and role in UC remain unknown. Here, we elucidate the function of miR-206 in the pathogenesis of UC. In patients with active-UC, miR-206 and adenosine A3 receptor (A3AR) levels were significantly upregulated and downregulated, respectively, and were inversely correlated. A3AR was expressed in the colon mucosa (particularly in colon epithelial-cell membranes). In HT-29 cells, miR-206 downregulated A3AR mRNA/protein expression by directly targeting the A3AR 3'-UTR; miR-206 overexpression and knockdown respectively increased and decreased TNF-α-induced nuclear NF-κB/p65, p-IκB-α, IKKα, p-IKKα and IL-8/IL-1β secretion. However, A3AR-siRNA reversed the miR-206 inhibitory effect. Furthermore, miR-206 increased dextran sodium sulphate-induced colitis severity (i.e., increased bodyweight loss, DAI score, colon shrinkage, and MPO activity), which was partially ameliorated by miR-206-antagomir treatment. miR-206-agomir treatment potently suppressed A3AR expression and increased NF-κB signalling and downstream cytokine (TNF-α/IL-8/IL-1β) expression in the mouse colon, in contrast to miR-206-antagomir administration. Taken together, our results demonstrated that miR-206 has a proinflammatory role in UC by downregulating A3AR expression and activating NF-κB signalling.
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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.