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<p>While metabolic reprogramming in cancer is well-documented, the epigenetic consequences of lactate accumulation—particularly histone lactylation—remain underexplored as a unifying mechanism driving immune evasion and therapy resistance. This review synthesizes emerging evidence that lactylation remodels the tumor microenvironment (TME) by polarizing macrophages, exhausting T cells, and stabilizing oncogenic transcripts. We highlight the dual roles of lactylation as both a metabolic sensor and a mediator of immunosuppression, underscoring its potential as a therapeutic target. Unresolved questions, such as context-dependent effects of specific lactylation sites (e.g., H3K18la and H3K9la) and the interplay with other post-translational modifications, are critically evaluated. We also propose strategies to exploit lactylation pathways for combination therapies. </p>

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Histone lactylation: a new target for overcoming immune evasion and therapy resistance

  • 期刊论文

  • 发表日期：

    2025年8月2日

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  • Fatemeh Ghadyani,
  • Pouyan Zandi,
  • Soudeh Ghafouri-Fard

摘要

While metabolic reprogramming in cancer is well-documented, the epigenetic consequences of lactate accumulation—particularly histone lactylation—remain underexplored as a unifying mechanism driving immune evasion and therapy resistance. This review synthesizes emerging evidence that lactylation remodels the tumor microenvironment (TME) by polarizing macrophages, exhausting T cells, and stabilizing oncogenic transcripts. We highlight the dual roles of lactylation as both a metabolic sensor and a mediator of immunosuppression, underscoring its potential as a therapeutic target. Unresolved questions, such as context-dependent effects of specific lactylation sites (e.g., H3K18la and H3K9la) and the interplay with other post-translational modifications, are critically evaluated. We also propose strategies to exploit lactylation pathways for combination therapies.