Findings show that GCN5-mediated lactylation reshapes tumor immune microenvironment, highlighting potential for effective cancer treatment.
• GCN5 mediates ERK K231 lactylation linking glycolysis to oncogenic MAPK signaling. • Targeting GCN5 lactylation offers a strategy to overcome resistance to MEK or ERK inhibitors. • Modulating lactylation reshapes the tumor immune microenvironment and enhances T cell function. • Inhibiting site-specific lactylation is a precise strategy for glycolytic RAS ERK driven cancers.
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Tzeng et al. (2026) studied this question.
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