Lactylation Drives Tumor Immune Evasion

1. Literature Information

This research elucidates a lactate–lactylation–METTL3–m6A–STAT3 signaling axis that remodels tumorinfiltrating myeloid cells and promotes immunosuppression, revealing a key mechanism of tumor immune escape.

2. Research Background

Tumor cells produce large amounts of lactate via aerobic glycolysis, shaping an immunosuppressive microenvironment. Lactylation is a novel histone modification using lactate as donor. However, how lactylation regulates immune cells and promotes tumor progression remains unclear.

3. Research Approach

Using clinical samples, animal models and cell biology, researchers investigated histone and nonhistone lactylation in myeloid cells. They explored transcriptional regulation of METTL3 by lactylation, m6A modification of Jak1 mRNA, and STAT3 pathway activation.

4. Research Outcomes

· Tumorderived lactate induces histone lactylation and upregulates METTL3 in myeloid cells.

· METTL3 mediates Jak1 mRNA m6A modification, enhancing translation via YTHDF1.

· Activated JAK1–STAT3 signaling drives immunosuppressive gene expression.

· Lactylation directly modifies METTL3 protein to enhance its enzymatic activity, forming a positive feedback loop.

· Myeloidspecific METTL3 knockout inhibits tumor growth in mice.

· High METTL3 correlates with poor prognosis in colorectal cancer patients.

5. Product Empowerment

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· Superior specificity with minimal crossreaction to acetylation, crotonylation and other acylations.

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6. Brand Mission

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