Mechanisms of FOXK1-regulated glycolipid metabolism in mediating TOX-induced histone lactylation to promote CD8⁺ T cell exhaustion in high-grade serous ovarian cancer

Key Points

• CD8⁺ T cell exhaustion is promoted by FOXK1-regulated histone lactylation, indicating a novel mechanism.
• Key evidence shows high TOX levels correlate with increased histone lactylation in cancer models.
• Mechanistic analysis explores FOXK1 and glycolipid metabolism's role in T cell fatigue processes.
• Understanding FOXK1's mechanism may provide new therapeutic strategies for treating ovarian cancer.