组蛋白乳酰化 (Hla) 是一种与代谢应激相关的组蛋白修饰，其特征在于特定的基因表达调节。然而，Hla 在肺腺癌 (LUAD) 发病机制中的作用仍有待探索。通过生物信息学分析，我们发现BZW2在LUAD组织中表达水平升高，这与不良预后相关。流式细胞术和TUNEL法分别用于分析LUAD细胞和组织的凋亡。分析细胞功能实验对LUAD细胞表型的影响。 XF 96细胞外通量分析仪测量ECAR值，并使用试剂盒检测乳酸产生和葡萄糖消耗。并进行了动物实验以进一步验证。细胞实验表明，BZW2 通过促进糖酵解介导的乳酸产生和 IDH3G 的乳酰化来促进 LUAD 的恶性进展。在令人信服的体内验证中，抑制 Hla 可以抑制 LUAD 的恶性进展。 BZW2 敲低与 2-DG 治疗相结合可显着抑制小鼠肿瘤生长。 BZW2可以通过糖酵解介导的IDH3G乳酰化调节LUAD的进展，为糖酵解和Hla靶向治疗LUAD提供理论基础。

Histone lactylation (Hla) is a metabolically stress-related histone modification that featured in specific gene expression regulation. However, the role of Hla in the pathogenesis of lung adenocarcinoma (LUAD) remains unexplored. Through bioinformatics analysis, we found that BZW2 exhibited an elevated level of expression in LUAD tissues, which was associated with a poor prognosis. Flow cytometry and TUNEL assay were used to analyze the apoptosis of LUAD cells and tissues, respectively. The effect of the cell function experiment on the LUAD cell phenotype was analyzed. An XF 96 Extracellular Flux Analyzer measured the ECAR value, and kits were used to detect lactate production and glucose consumption. Animal experiments were performed for further verification. Cell experiments showed that BZW2 fostered the malignant progression of LUAD by promoting glycolysis-mediated lactate production and lactylation of IDH3G. In a compelling in vivo validation, the inhibition of Hla could suppress the malignant progression of LUAD. Knockdown of BZW2 combined with 2-DG treatment significantly repressed tumor growth in mice. BZW2 could regulate the progression of LUAD through glycolysis-mediated IDH3G lactylation, offering a theoretical basis for the targeted treatment of LUAD with glycolysis and Hla.