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Background <p>Gastric cancer (GC) remains a leading cause of cancer-related mortality globally, with current immunotherapies exhibiting limited therapeutic efficacy owing to the immunosuppressive tumour microenvironment (TME).</p> Main body <p>Lactate, a hallmark metabolic by-product of tumour glycolysis, also functions as a critical metabolic driver. By promoting TME acidification, immunosuppression, and epigenetic reprogramming, lactate emerges as a pivotal regulator in reshaping GC immune evasion and therapeutic resistance, while also strongly correlating with chemotherapy resistance. Furthermore, the dysregulated expression of lactate-associated metabolic genes represents a promising therapeutic target.</p> Conclusion <p>This review elucidates the dual roles and clinical value of lactate in gastric cancer as both an energy substrate and a signalling molecule within the tumour microenvironment and positions lactylation as a critical metabolic–epigenetic bridge. We also discuss innovative strategies that integrate lactate metabolism-targeting immune checkpoint inhibitors to overcome therapeutic resistance in GC.</p>

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Lactate and gastric cancer immunotherapy from regulatory mechanisms to therapeutic strategies: a critical review

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月14日

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  • Yuanzhu Hao,
  • Yanan Zhang,
  • Yu Zhang,
  • Duo Yang,
  • Dan Ren,
  • Yixing Yue,
  • Qian Li,
  • QingLing Fan,
  • Chao Sun,
  • Manli Cui,
  • Mingxin Zhang

摘要

Background

Gastric cancer (GC) remains a leading cause of cancer-related mortality globally, with current immunotherapies exhibiting limited therapeutic efficacy owing to the immunosuppressive tumour microenvironment (TME).

Main body

Lactate, a hallmark metabolic by-product of tumour glycolysis, also functions as a critical metabolic driver. By promoting TME acidification, immunosuppression, and epigenetic reprogramming, lactate emerges as a pivotal regulator in reshaping GC immune evasion and therapeutic resistance, while also strongly correlating with chemotherapy resistance. Furthermore, the dysregulated expression of lactate-associated metabolic genes represents a promising therapeutic target.

Conclusion

This review elucidates the dual roles and clinical value of lactate in gastric cancer as both an energy substrate and a signalling molecule within the tumour microenvironment and positions lactylation as a critical metabolic–epigenetic bridge. We also discuss innovative strategies that integrate lactate metabolism-targeting immune checkpoint inhibitors to overcome therapeutic resistance in GC.