ArticleCell reports2024
Metabolic reprogramming by histone deacetylase inhibition preferentially targets NRF2-activated tumors.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 20 citations in OpenAlex.
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- Developmental Extracellular Matrix as a Bioactive Niche for Spinal Cord Organoid Maturation and SCI Repair.Molecular neurobiology · 2026Review
- Silencing SGO2 by Oxamic Acid Dissociates Glycolysis and BRCA1-Mediated DNA Repair to Improve the Chemosensitivity of Lung Adenocarcinoma.Exploration (Beijing, China) · 2026Article
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- Disengaging the Engine: Histone Deacetylases 1 and 2-Mediated Acetylation of Hexokinase-2 Regulates Energy Metabolism in Microglia Following Intracerebral Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- From metabolism to genome integrity: NRF2 as a key mediator of cancer therapy response.Frontiers in cell and developmental biology · 2026Review
- [Inhibition of BRD4 promotes migration of esophageal squamous cell carcinoma cells with low ACC1 expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Article
- Targeting glucose transporters in parkinson's disease: a novel metabolic approach for disease modification.Metabolic brain disease · 2025Review
- NRF2 supports non-small cell lung cancer growth independently of CBP/p300-enhanced glutathione synthesis.EMBO reports · 2025Article
- Lymphatic Metastasis of Esophageal Squamous Cell Carcinoma: The Role of NRF2 and Therapeutic Strategies.Cancers · 2025Review
- GepA, a GGDEF-EAL protein, regulates biofilm formation and swimming motility in Vibrio parahaemolyticus.Archives of microbiology · 2025Article
- Targeting Epigenetic Dysregulations in Head and Neck Squamous Cell Carcinoma.Journal of dental research · 2025Review
- Metabolism-driven chromatin dynamics: Molecular principles and technological advances.Molecular cell · 2025Review
- Cotton GhMAX2 promotes single-celled fiber elongation by releasing the GhS1FA-mediated inhibition of fatty acid biosynthesis.Plant cell reports · 2025Article
- The impact of oxidative stress and the NRF2-KEAP1-ARE signaling pathway on anticancer drug resistance.Oncology research · 2025Review
- The Potential of Nanotechnology in Anti-cancer Drug to Regulate Nrf2 Signaling for Cancer Therapeutic Purposes.Current medicinal chemistry · 2025Review
- Cuproptosis and Cu: a new paradigm in cellular death and their role in non-cancerous diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Progress and Gaps in Respiratory Disease Research and Treatment: Highlights of the IRM 2024 in Shanghai.Journal of respiratory biology and translational medicine · 2024Article
- Inhibition of glutaminolysis alone and in combination with HDAC inhibitor has anti-myeloma therapeutic effects.Cancer drug resistance (Alhambra, Calif.) · 2024Article
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Authors and funding
13 authors at 4 institutions in 1 country.
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Abstract
The interplay between metabolism and chromatin signaling is implicated in cancer progression. However, whether and how metabolic reprogramming in tumors generates chromatin vulnerabilities remain unclear. Lung adenocarcinoma (LUAD) tumors frequently harbor aberrant activation of the NRF2 antioxidant pathway, which drives aggressive and chemo-resistant disease. Using a chromatin-focused CRISPR screen, we report that NRF2 activation sensitizes LUAD cells to genetic and chemical inhibition of class I histone deacetylases (HDACs). This association is observed across cultured cells, mouse models, and patient-derived xenografts. Integrative epigenomic, transcriptomic, and metabolomic analysis demonstrates that HDAC inhibition causes widespread redistribution of H4ac and its reader protein, which transcriptionally downregulates metabolic enzymes. This results in reduced flux into amino acid metabolism and de novo nucleotide synthesis pathways that are preferentially required for the survival of NRF2-active cancer cells. Together, our findings suggest NRF2 activation as a potential biomarker for effective repurposing of HDAC inhibitors to treat solid tumors.
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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.