ArticleiLIVER2026
Histone delactylation shapes epigenetic landscapes and therapeutic stratification in hepatocellular carcinoma.
Article in iLIVER, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and aims: Histone lysine lactylation has emerged as a key epigenetic link between metabolism and gene regulation. Its homeostasis depends on both lactylation and delactylation. The biological and clinical relevance of histone lysine delactylation in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate the clinical relevance of histone lysine delactylation (HLDL) in hepatocellular carcinoma and to establish an HLDL-based molecular classification for precision therapy. Methods: We systematically profiled HLDL across multi-omics HCC cohorts ( Results: The HLDL classification delineated two major subtypes with distinct biological and therapeutic profiles. Low-HLDL tumors displayed higher genomic instability, activated oncogenic signaling, and an immune-infiltrated yet suppressive microenvironment, corresponding to poorer outcomes but higher sensitivity to immune checkpoint inhibitors, atezolizumab plus bevacizumab therapy, and sorafenib. In contrast, high-HLDL tumors exhibited a metabolically stable and delactylation-active phenotype, responding more favorably to lenvatinib and transarterial chemoembolization. Functional experiments confirmed that reduced HLDL activity led to elevated histone lysine lactylation, PD-L1 upregulation, and lenvatinib resistance, whereas restoring delactylation reversed these effects. Conclusions: Histone lysine delactylation constitutes a critical epigenetic determinant of HCC heterogeneity and therapeutic response. The HLDL-based classification developed in this study integrates metabolic, immune, and pharmacologic features into a concise framework, offering new avenues for precision therapy and potential targets for modulating the lactylation-delactylation balance in HCC.
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