ArticleNature communications2025
SOX2 drives esophageal squamous carcinoma by reprogramming lipid metabolism and histone acetylation landscape.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Epigenomic Remodeling by Lipid Metabolism: A Cross-Disease Perspective on Cancer and Brain Disorders.Genes · 2026Review
- Whole-body mass spectrometry imaging reveals metabolome and lipid peroxidation heterogeneity in zebrafish xenografts of esophageal squamous cell carcinoma.Analytical and bioanalytical chemistry · 2026Article
- Comparative single cell analysis of wound and cancer identifies the metabolic dialogues between tumor initiating stem cells and macrophages.bioRxiv : the preprint server for biology · 2026Article
- Advances in epigenetic therapy for esophageal cancer.Clinical epigenetics · 2026Review
- Review
- Rewiring immunity in rheumatoid arthritis: metabolic and epigenetic therapeutic strategies.Frontiers in pharmacology · 2026Review
- The Dysregulation of Lysine Acetylation in Esophageal Squamous Cell Carcinoma: Mechanisms, Therapeutic Targets and Clinical Perspectives.Technology in cancer research & treatmentReview
Corrections and comments
- Erratum issued
Authors and funding
17 authors.
Funding
Abstract
SOX2 is a potent oncodriver for various squamous cancers, but the underlying mechanism is largely unknown. Here we uncover a role of SOX2 in promoting global histone acetylation in esophageal squamous cancer cells (ESCCs). Mechanistic studies reveal that SOX2 promotes global histone acetylation in an AKT-independent manner, and does so by promoting histone acetylation at both SOX2 binding and non-SOX2 binding sites, and accounts for the formation of about half of the super-enhancers. Combined metabolic and transcriptional analyses reveal two mechanisms by which SOX2 enhances global histone acetylation: promoting the expression of multiple histone acetyltransferases and reducing acetyl-CoA consuming fatty acid synthesis in part by repressing the expression of ACSL5. Finally, SOX2 expression correlates negatively with ACSL5 and positively with histone acetylation in clinical esophageal squamous tumors. Altogether, our study uncovers a role of SOX2 in reprogramming lipid metabolism and driving histone hyperacetylation and super-enhancer function, providing mechanistic insights of SOX2 acting as a potent oncodriver.
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Registered trials
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