ReviewFrontiers in immunology2026
The glycolysis-lactylation axis: a metabolic-epigenetic driver of immunosuppression and therapy resistance in cancer.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Rewiring glucose metabolism in pancreatic cancer by natural compounds: implications for immune evasion and therapeutic targets.Molecular biology reports · 2026Review
- DNER drives glycolytic reprogramming in renal cell carcinoma by activating the JAK2/STAT3 signaling pathway.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
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Abstract
Background: The immunosuppressive tumor microenvironment (TME) is a major barrier to the efficacy of cancer immunotherapy. Tumor metabolic reprogramming, particularly aerobic glycolysis (the Warburg effect), drives lactate accumulation in the TIME. Beyond fueling tumor growth, lactate-derived lysine lactylation (Kla) has emerged as a pivotal epigenetic and post-translational modifier, directly coupling metabolic activity to the regulation of immune cell function and tumor cell resilience. Main body: This review synthesizes current evidence to delineate how the glycolysis-lactylation axis orchestrates a multi-faceted immunosuppressive program and confers broad therapy resistance. We detail its mechanisms in: (1) Inhibiting antitumor immunity by driving M2 macrophage polarization, enhancing regulatory T cell (Treg) function, and promoting CD8 Conclusions: Targeting the lactate-lactylation signaling hub represents a promising metabolic-epigenetic strategy to dismantle tumor-driven immunosuppression and overcome therapeutic resistance, particularly resistance to immunotherapy. Although a substantial body of preclinical evidence, ranging from cancer cell line models to patient-derived xenografts, supporting the potential of targeting this axis, its clinical translation remains hindered by a gap in the evidence hierarchy, necessitating further validation through prospective clinical trials.
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