ArticleFrontiers in pharmacology2022
Nintedanib Alleviates Experimental Colitis by Inhibiting CEBPB/PCK1 and CEBPB/EFNA1 Pathways.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
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- Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate.Cellular and molecular life sciences : CMLS · 2026Article
- Diagnostic and prognostic significance of Super-enhancer-associated genes in Crohn's disease and immune regulatory roles.European journal of medical research · 2025Article
- Role of glycolysis related genes in the pathogenesis of hemorrhoids and immune cell infiltration analysis.Scientific reports · 2025Article
- Yi-Fei-Tong-Bi Decoction Alleviates Bleomycin Induced Pulmonary Fibrosis in Mice.Drug design, development and therapy · 2025Article
- Fibroblast Heterogeneity in Inflammatory Bowel Disease.International journal of molecular sciences · 2024Review
- Key Disease-Related Genes and Immune Cell Infiltration Landscape in Inflammatory Bowel Disease: A Bioinformatics Investigation.International journal of molecular sciences · 2024Article
- Transcriptomic Analysis of PDCoV-Infected HIEC-6 Cells and Enrichment Pathways PI3K-Akt and P38 MAPK.Viruses · 2024Article
- Latent inter-organ mechanism of idiopathic pulmonary fibrosis unveiled by a generative computational approach.Scientific reports · 2023Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The super-enhancer, a cluster of enhancers with strong transcriptional activity, has become one of the most interesting topics in recent years. This study aimed to investigate pathogenic super-enhancer-driven genes in IBD and screen therapeutic drugs based on the results. In this study, through the analysis of differentially expressed genes in colitis patients from the GEO database and the analysis of the super-enhancer-associated database, we found that the super-enhancer pathogenic genes PCK1 and EFNA1 were simultaneously regulated by transcription factor CEBPB through two super-enhancers (sc-CHR20-57528535 and sc-CHR1-155093980). Silencing CEBPB could significantly inhibit the expression of PCK1 and EFNA1 and enhance the expression of epithelial barrier proteins claudin-1, occludin, and ZO-1. In LPS-induced Caco-2 cells, drugs commonly used in clinical colitis including tofacitinib, oxalazine, mesalazine, and sulfasalazine inhibited mRNA levels of CEBPB, PCK1, and EFNA1. In the drug screening, we found that nintedanib significantly inhibited the mRNA and protein levels of CEBPB, PCK1, and EFNA1.
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