免疫逃逸和代谢重编程是癌症的两个重要标志。 Mucin-16 (MUC16) 与不同癌症中的糖酵解和免疫反应有关。然而，其与鼻咽癌（NPC）的关系尚未得到很好的描述。我们试图剖析MUC16在鼻咽癌中的功能和详细机制。进行生物信息学预测以鉴定NPC相关分子。 MUC16在鼻咽癌组织中显着增强，这与患者的肿瘤分期晚期相关。慢病毒质粒介导的MUC16缺失抑制了NPC细胞的恶性行为，MUC16缺失对糖酵解的抑制阻止了NPC细胞的免疫逃逸。 E74 样因子 3 (ELF3) 与 MUC16 启动子结合，促进 MUC16 的转录。 MUC16过表达逆转了ELF3沉默对NPC糖酵解和免疫逃逸的抑制作用，并加速体内肿瘤生长。 ELF3 在 NPC 中的过度表达与其启动子中 DNA 甲基化的减少有关。我们的研究结果揭示了ELF3/MUC16轴在鼻咽癌免疫逃逸和代谢重编程中的作用，为鼻咽癌提供了潜在的治疗靶点。

Immune escape and metabolic reprogramming are two essential hallmarks of cancer. Mucin-16 (MUC16) has been linked to glycolysis and immune response in different cancers. However, its involvement in nasopharyngeal carcinoma (NPC) has not been well described. We seek to dissect the functions and detailed mechanisms of MUC16 in NPC. Bioinformatics prediction was performed to identify NPC-related molecules. MUC16 was significantly enhanced in NPC tissues, which was correlated with the advanced tumor stage of patients. Lentiviral plasmids-mediated MUC16 deletion inhibited the malignant behavior of NPC cells, and glycolysis inhibition by MUC16 deletion blocked immune escape in NPC cells. E74-like factor 3 (ELF3) bound to the MUC16 promoter to promote transcription of MUC16. MUC16 overexpression reversed the repressive effect of ELF3 silencing on glycolysis and immune escape in NPC and accelerated tumor growth in vivo. Overexpression of ELF3 in NPC was associated with reduced DNA methylation in its promoter. Our findings revealed the role of the ELF3/MUC16 axis in the immune escape and metabolic reprogramming of NPC, providing potential therapeutic targets for NPC.