Targeted-therapy failure in treating nonsmall cell lung cancer (NSCLC) frequently occurs because of the emergence of drug resistance and genetic mutations. The same mutations also result in aerobic glycolysis, which further antagonizes outcomes by localized increases in lactate, an immune suppressor. Recent evidence indicates that enzymatic lowering of lactate can promote an oncolytic immune microenvironment within the tumour. Here, we review factors relating to lactate expression in NSCLC and the utility of lactate oxidase (LOX) for governing therapeutic delivery, its role in lactate oxidation and turnover, and relationships between lactate depletion and immune cell populations. The lactate-rich characteristic of NSCLC provides an exploitable property to potentially improve NSCLC outcomes and design new therapeutic strategies to integrate with conventional therapies.

由于耐药性和基因突变的出现，治疗非小细胞肺癌（NSCLC）的靶向治疗失败经常发生。同样的突变也会导致有氧糖酵解，通过局部增加乳酸（一种免疫抑制剂）来进一步对抗结果。最近的证据表明，酶促降低乳酸可以促进肿瘤内的溶瘤免疫微环境。在这里，我们回顾了与 NSCLC 中乳酸表达相关的因素以及乳酸氧化酶 (LOX) 在控制治疗递送中的作用、其在乳酸氧化和周转中的作用，以及乳酸消耗与免疫细胞群之间的关系。