ReviewOncology letters2026
Lactylation enzymes in cancer: Mechanisms and novel therapeutic approaches (Review).
Review in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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8 authors.
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Abstract
Metabolic reprogramming, particularly the Warburg effect, drives tumor progression not only by supplying energy but also by reshaping the epigenetic landscape through lysine lactylation. The present review summarizes the molecular organization of the lactylation regulatory network, highlighting two distinct writer mechanisms: i) A classical acyl-coenzyme A (acyl-CoA)-dependent pathway mediated by the MYST (MOZ, Ybf2/Sas3, Sas2 and Tip60) family; and ii) a recently described acyl-CoA-independent pathway driven by the metabolic sensors, alanyl-tRNA synthetases 1 and 2. The present review further explains how these 'writers', together with specific 'erasers' and 'readers', convert intracellular lactate accumulation into stable transcriptional programs that support immunosuppression, metabolic plasticity and therapeutic resistance. In addition, the current review discusses emerging therapeutic strategies targeting this axis, shifting from broad lactate metabolism inhibition towards more precise approaches that reduce the off-target toxicity of conventional epigenetic drugs. Finally, the present review outlines lactylation-associated gene signatures as potential biomarkers, providing a framework for the development of metabolic-epigenetic therapies.
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