Lactylation couples glycolysis with cell cycle progression in cancer cells.

Lactate-dependent lactylation of PGK1 at K131 activates Aurora B via T232 phosphorylation, promoting mitotic progression in cancer cells.

• Why it matters: Aurora B is required for mitosis, but how tumour metabolism regulates its activity is unclear. Linking glycolytic output to mitotic control could reveal actionable vulnerabilities.
• What they did: Cells with increased aerobic glycolysis generate lactate that enables KAT2A-mediated lactylation of PGK1 at K131, which then phosphorylates Aurora B at T232. Disrupting this axis using PGK1 K131R or an Aurora B–binding–defective PGK1 variant was tested alongside a peptide blocking PGK1–Aurora B with anti-PD-1.
• The result: Blocking the pathway causes mitotic defects and cGAS-STING activation, suppressing tumour proliferation and inhibiting tumour growth in mice. The PGK1–Aurora B–disrupting peptide plus anti-PD-1 increases CD8+ T-cell infiltration and yields synergistic anti-tumour effects.

AI summary of the abstract · may contain errors · not medical advice · read the paper.