ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Super-enhancer Activates Master Transcription Factor NR3C1 Expression and Promotes 5-FU Resistance in Gastric Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- A Non-Canonical Core Transcriptional Regulatory Circuit Orchestrates Chromatin Reprogramming to Drive Osimertinib Resistance in Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting the NR3C1-ACSL4 Axis Triggers Ferroptosis to Overcome Radioresistance in Prostate Cancer.Cancer science · 2026Article
- NR3C1 Modulates Wnt Signalling to Influence the Invasiveness and Immune Features of Nonfunctioning Invasive Pituitary Adenomas.Journal of cellular and molecular medicine · 2026Article
- Article
- Association ofTranslational cancer research · 2026Article
- TK1 in gastric cancer: Helicobacter pylori-driven oncogenesis biomarker, utility, and emerging targeted therapies.Frontiers in oncology · 2026Review
- The prognostic marker NRIP1 is associated with tumor progression and immune infiltration in acute myeloid leukemia.Acta biochimica et biophysica Sinica · 2025Article
- SETD6 mediates selective interaction and genomic occupancy of BRD4 and MITF in melanoma cells.NAR cancer · 2025Article
- Super-enhancer Activates Master Transcription Factor NR3C1 Expression and Promotes 5-FU Resistance in Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Liquid-liquid phase separation in super enhancer-driven oncogenesis: mechanisms, immune evasion, and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- KLF5 promotes tumor proliferation and oxaliplatin resistance via chromatin remodeling in KRAS-mutated colorectal cancer.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- TGM2 regulated by transcription factor NR3C1 drives p38 MAPK-mediated tumor progression and immune evasion in lung squamous cell carcinoma.Frontiers in immunology · 2025Article
- Combinational Analysis of Metabolomic and O-GlcNAcylation Omics Reveals the HBP Metabolic Regulation of Chemoresistance via GFPT1/NR3C1 O-GlcNAcylation/GPX4 Axis.Research (Washington, D.C.) · 2025Article
- Super-enhancer-associated LINC00963 promotes metastasis of gastric cancer through epithelial-mesenchymal transition.PloS one · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
Poor response to 5-fluorouracil (5-FU) remains an obstacle in the treatment of gastric cancer (GC). Super enhancers (SEs) are crucial for determining tumor cell survival under drug pressure. SE landscapes related to 5-FU-resistance are mapped to GC using chromatin immunoprecipitation-sequencing (ChIP-Seq). SiRNA transcription factors (TFs) screen determines master TF Nuclear Receptor Subfamily 3 Group C Member 1 (NR3C1) activated by SE. High NR3C1 expression driven by SE correlated with 5-FU resistance in patient-derived organoids (PDOs). Phase separation formed by NR3C1 is observed using fluorescence recovery after photobleaching (FRAP). NR3C1 protein and Mediator promoted SE-related gene transcription via phase separation. SEs and NR3C1 co-binding patterns are explored using Cleavage Under Targets and Tagmentation (CUT&Tag) sequencing. 5-FU-related genes driven by NR3C1 are identified using epigenetic reader inhibitor JQ1 and NR3C1 specific inhibitor Cort108297. NR3C1 knockdown increases 5-FU sensitivity and alters the SE landscape through enhancer reprogramming, reducing downstream 5-FU-related target genes. JQ1 and Cort108297 both improve 5-FU efficacy in PDOs and patient-derived xenografts (PDXs) by destroying SEs or inhibiting NR3C1. In conclusion, SE-driven NR3C1 promotes 5-FU resistance in GC. SE destruction and NR3C1 inhibition lead to enhancer reconstruction and reduce 5-FU-related gene transcription, providing alternative therapeutic strategies for improving 5-FU sensitivity.
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