ArticleJournal of translational medicine2025
H2BC9 lactylation modulates esophageal squamous cell carcinoma progression via the Wnt/β-catenin signaling pathway.
Article in Journal of translational medicine, 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.
- Review
- Non-structural maintenance of chromosome condensin I complex subunit H knockdown suppresses malignant progression of esophageal squamous cell carcinoma via the Wnt/β-catenin signaling pathway.Journal of gastrointestinal oncology · 2026Article
- Lactylation Modification and Esophageal Cancer: Research Progress From Hypoxia-Induced Metabolic Reprogramming to Immune Escape.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Lactate metabolism and protein lactylation in inflammatory and tumor microenvironments.Molecular biomedicine · 2026Review
- Lysine l-Lactylation: Bridging Metabolism, Chromatin and Disease.Cell proliferation · 2026Review
- Integrative analysis of HMGB3 in esophageal carcinoma: expression profile, prognostic significance, and immune microenvironment associations.Translational cancer research · 2026Article
- Identification ofTranslational cancer research · 2026Article
- Precision immunotherapy in oesophageal squamous cell carcinoma: Molecular pathogenesis and checkpoint inhibitor response prediction.World journal of gastrointestinal pharmacology and therapeutics · 2026Review
- Honokiol attenuates renal fibrosis via SIRT3-Mediated regulation of Wnt/β-Catenin signaling.Functional & integrative genomics · 2026Article
- Advances in epigenetic therapy for esophageal cancer.Clinical epigenetics · 2026Review
- Acute myeloid leukemia (AML)-derived bone mesenchymal stem cell exosomal METTL14 promotes AML cell growth and glycolysis by HOXA3/WNT7B axis.Cell biology and toxicology · 2026Article
- Research progress on protein lactylation in female reproductive disease: molecular mechanisms, functions, and therapeutic implications.Frontiers in pharmacology · 2026Review
- IGFBP1 is a prognostic biomarker in esophageal carcinoma: mechanistic insights from bioinformatics profiling toFrontiers in immunology · 2026Article
- Lactylation in digestive system tumors: from mechanisms to therapeutic target.Frontiers in oncology · 2025Review
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10 authors.
Funding
Abstract
backgroundLactate, traditionally regarded as a metabolic waste product of glycolysis, has recently emerged as a critical signaling molecule and epigenetic modifier via protein lactylation. However, the functional consequences of histone lactylation in cancer progression remain poorly understood.
methodsWe integrated transcriptomic data from TCGA and GEO (GSE188900) with bulk and single-cell RNA-seq analyses to identify lactylation-associated histone variants involved in esophageal squamous cell carcinoma (ESCC). Functional assays, immunoprecipitation (IP), western blotting (WB), chromatin immunoprecipitation (ChIP)-qPCR, and luciferase reporter assays were employed to investigate the role of H2BC9 and its lactylation in ESCC. A xenograft tumor model was used to validate in vivo relevance.
resultsWe identified H2BC9, a histone H2B variant, as a lactylation-associated oncogene that is overexpressed in ESCC and correlates with poor prognosis. Lactate stimulation induced H2BC9 lactylation, particularly at lysine 44 (K44), as confirmed by mass spectrometry and IP-WB assays. Mechanistically, K44 lactylation of H2BC9 enhanced the transcriptional activity of Wnt7b, leading to activation of the Wnt/β-catenin pathway. Mutation of K44 (K44R) abolished H2BC9 lactylation and significantly impaired its ability to promote ESCC cell proliferation and Wnt7b transcription, as demonstrated by ChIP-qPCR and dual-luciferase assays. In vivo, H2BC9 K44R-expressing cells exhibited reduced tumor growth in xenograft models. Furthermore, H2BC9 expression was associated with an immunosuppressive tumor microenvironment and chemoresistance.
conclusionOur study reveals a novel regulatory axis in which H2BC9 K44 lactylation activates Wnt7b transcription and downstream Wnt/β-catenin signaling, driving ESCC progression. Targeting H2BC9 lactylation may offer a promising therapeutic strategy to overcome tumor growth and immune evasion in ESCC.
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