The study aims to elucidate the role of HIF-1α K172 lactylation in hypoxia-mediated immune evasion in esophageal squamous cell carcinoma.
Identified lactylation at K172 of HIF-1α in esophageal squamous cell carcinoma tissues.
Investigated the impact on T cell cytotoxicity and immune response due to hypoxic conditions.
Proposed lactylation as a potential therapeutic strategy to enhance immunotherapy outcomes.
HIF-1α K172 lactylation significantly correlates with reduced T cell cytotoxicity.
Observed immune evasion mechanisms are tightly linked to lactylation levels.
Suggests targeting HIF-1α lactylation could enhance the effectiveness of immunotherapy.
Abstract
T cell cytotoxicity. Our study identifies HIF-1α K172 lactylation as a pivotal mechanism of hypoxia-mediated immune escape in ESCC, suggesting a therapeutic strategy to improve immunotherapy.