ArticleCell death and differentiation2026
BRD9 recognizes lactate-induced H3K18 lactylation to drive oncogenic chromatin remodeling in hepatocellular carcinoma.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Targeting lactylation in hepatocellular carcinoma: Mechanistic insights and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Clinical implications of lactylation modification in digestive system tumors (Review).Oncology letters · 2026Review
- Article
- Computational Discovery of Dual-Target LDHA/BRD4 Inhibitors Targeting the Lactate-Kla-B7-H3 Immunosuppressive Axis Through AI-Driven Virtual Screening.Pharmaceuticals (Basel, Switzerland) · 2026Article
- When metabolic enzymes meet lactylation: a bidirectional dialogue in health and disease.Frontiers in cell and developmental biology · 2026Review
- Histone lactylation: a metabolic-epigenetic bridge linking glycolysis to salivary gland fibrosis in Sjögren's disease.Frontiers in immunology · 2026Review
- STAT3 at the tumor-immune interface: mechanisms of immune escape and therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Histone lactylation couples glycolytic metabolism to oncogenic transcription, but its mechanistic readers remain poorly defined. Here, we identify bromodomain-containing protein 9 (BRD9) as a lactyl-lysine reader that links lactate-driven H3K18 lactylation (H3K18la) to chromatin remodeling in hepatocellular carcinoma (HCC). Clinically, elevated H3K18la levels correlate with poor HCC prognosis. Structural (NMR) and biophysical analyses demonstrate that BRD9's bromodomain engages H3K18la with weak, transient affinity through its conserved acetyl-lysine pocket, distinct from its stable H3K18ac binding. This enables BRD9 to function as a metabolic-epigenetic sensor, dynamically recruited to chromatin in response to glycolytic flux. Multi-omics profiling reveals that H3K18la recruits BRD9 and the non-canonical BRG1-associated factor (ncBAF) chromatin remodeling complex to active enhancers and promoters, promoting chromatin accessibility and driving oncogenic transcription (SPARC, TMEM64, ANGEL1, SCARB1). Glycolytic inhibition or BRD9 targeting displaces BRD9 from chromatin, suppresses oncogenes, and impairs HCC proliferation. Modulating the lactylation vis p300 or HDAC inhibition attenuates transcription and reduces tumor viability. In vivo, glycolytic inhibition suppresses tumor growth. Our findings establish a feedforward loop wherein glycolytic flux promotes H3K18la-dependent BRD9-ncBAF recruitment to remodel chromatin and sustain oncogenic transcription, defining BRD9 as a critical metabolic-epigenetic mediator and a promising therapeutic target in HCC.
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Registered trials
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