ArticleImmunologic research2015
Epithelial-specific ETS-1 (ESE1/ELF3) regulates apoptosis of intestinal epithelial cells in ulcerative colitis via accelerating NF-κB activation.
Article in Immunologic research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Epigenetic memory of colitis promotes tumour growth.Nature · 2026Article
- ELF3 promotes hyperglycemia-induced corneal epithelial senescence and IL-2 attenuates ELF3-associated signaling.Frontiers in molecular biosciences · 2026Article
- SIAE-Mediated Loss of Sialic Acid Acetylation Contributes to Ulcerative Colitis.Journal of inflammation research · 2025Article
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- Role of Aging in Ulcerative Colitis Pathogenesis: A Focus on ETS1 as a Promising Biomarker.Journal of inflammation research · 2025Article
- Immunosuppression and phenotypic plasticity in an atlas of human hepatocholangiocarcinoma.Hepatobiliary surgery and nutrition · 2024Article
- Investigation of the mutual crosstalk between ER stress and PI3K/AKT/mTOR signaling pathway in iron overload-induced liver injury in chicks.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Article
- multi-GPA-Tree: Statistical approach for pleiotropy informed and functional annotation tree guided prioritization of GWAS results.PLoS computational biology · 2023Article
- ESE-1 mediates lipopolysaccharide-induced BV2 cell inflammation via upregulation of HMGB1 expression.Journal of biosciences · 2023Article
- Prevention of ulcerative colitis by Huangqin decoction: reducing the intestinal epithelial cell apoptosis rate through the IFN-γ/JAK/ETS signalling pathway.Pharmaceutical biology · 2022Article
- Effects of miR-939 and miR-376A on ulcerative colitis using a decoy strategy to inhibit NF-κB and NFAT expression.European journal of histochemistry : EJH · 2022Article
- CDK11 Promotes Cytokine-Induced Apoptosis in Pancreatic Beta Cells Independently of Glucose Concentration and Is Regulated by Inflammation in the NOD Mouse Model.Frontiers in immunology · 2021Article
- Conditioned medium from adipose-derived stem cells attenuates ischemia/reperfusion-induced cardiac injury through the microRNA-221/222/PUMA/ETS-1 pathway.Theranostics · 2021Article
- Mesenchymal stem cell-derived exosomal microRNA-136-5p inhibits chondrocyte degeneration in traumatic osteoarthritis by targeting ELF3.Arthritis research & therapy · 2020Article
- Introducing GATA3 as a prominent player in Crohn's disease.Gastroenterology and hepatology from bed to bench · 2020Article
- Epithelial tumor suppressor ELF3 is a lineage-specific amplified oncogene in lung adenocarcinoma.Nature communications · 2019Article
- ESE1 expression correlates with neuronal apoptosis in the hippocampus after cerebral ischemia/reperfusion injury.Neural regeneration research · 2019Article
- FKBP11 protects intestinal epithelial cells against inflammation‑induced apoptosis via the JNK‑caspase pathway in Crohn's disease.Molecular medicine reports · 2018Article
- Jagged-1 attenuates LPS-induced apoptosis and ROS in rat intestinal epithelial cells.International journal of clinical and experimental pathology · 2018Article
- Genomic dissection of conserved transcriptional regulation in intestinal epithelial cells.PLoS biology · 2017Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-specific ETS-1 (ESE1), also named as ELF3, ERT and ESX, belonging to the ETS family of transcription factors, exerts multiple activities in inflammation, epithelial differentiation and cancer development. Previous data demonstrated that ESE1 synergizes with NF-κB to induce inflammation and drive tumor progress, and the nuclear translocation of ESE1 promotes colon cells apoptosis. However, the expression and biological functions of ESE1 in ulcerative colitis (UC) remain unclear. In this study, we reported for the first time that ESE1/ELF3 was over-expressed in intestinal epithelial cells (IECs) of patients with UC. In DSS-induced colitis mouse models, we observed the up-regulation of ESE1/ELF3 accompanied with the elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and NF-κB activation indicators [phosphorylated NF-κB p65 subunit (p-p65) and p-IκB] in colitis IECs. Increased co-localization of ESE1/ELF3 with active caspase-3 (and p-p65) in IECs of the DSS-induced colitis group further indicated the possible involvement of ESE1/ELF3 in NF-κB-mediated IEC apoptosis in UC. Employing the TNF-α-treated HT-29 cells as an IEC apoptosis model, we confirmed the positive correlation of ESE1/ELF3 with NF-κB activation and caspase-dependent IEC apoptosis in vitro. Immunoprecipitation and immunofluorescence assay revealed the physical interaction and increased nuclear translocation of ESE1/ELF3 and the NF-κB p65 subunit in TNF-α-treated HT-29 cells. Knocking ESE1/ELF3 down by siRNA significantly alleviated TNF-α-induced NF-κB activation and cellular apoptosis in HT-29 cells. Taken together, our data suggested that ESE1/ELF3 may promote the UC progression via accelerating NF-κB activation and thus facilitating IEC apoptosis.
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