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Article Abstract
Background: Endogenous retrovirus group E member 1 (EVA1A) is expressed in various normal tissues and plays a role in tumor development. However, its function in esophageal squamous cell carcinoma (ESCC) and immune regulation remains unclear.
Research Design And Methods: Bioinformatics, clinical samples, and in vivo/in vitro experiments were used to evaluate EVA1A expression and function. A co-culture system with CD8 T cells, as well as a xenograft mouse model, was established. CD8 T cell activity, glycolysis markers, lactate levels, and PLAU expression were assessed through flow cytometry, quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent (ELISA), lactate dehydrogenase (LDH) assays, and chromatin immunoprecipitation (ChIP).
Results: EVA1A was upregulated in ESCC and negatively correlated with CD8 T cell infiltration. EVA1A knockdown suppressed tumor growth and immune escape by reducing glycolysis and lactate production. Lactate promoted histone H4K12la lactylation, enhancing plasminogen activator-urokinase (PLAU) expression. PLAU overexpression reversed CD8 T cell activation induced by EVA1A silencing.
Conclusion: High EVA1A expression enhances glycolysis in ESCC, and the resulting lactate further induces H4K12la lactylation and promotes PLAU expression. This inhibits the anti-tumor activity of CD8 T cells, suggesting that EVA1A has potential as a therapeutic target for ESCC.
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| http://dx.doi.org/10.1080/1744666X.2025.2545904 | DOI Listing |
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