Liao, Zi-XianZi-XianLiaoKempson, Ivan MIvan MKempsonHsieh, Chia-ChenChia-ChenHsiehS.-JA TSENGPAN-CHYR YANG2021-11-022021-11-022021-07-2713596446https://scholars.lib.ntu.edu.tw/handle/123456789/586051Targeted-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.enLactate; Lactate oxidase; NSCLC; Nanoparticles; Nonsmall cell lung cancer; Tumor microenvironment[SDGs]SDG3lactate 2 monooxygenase; lactic acid; cancer resistance; cancer therapy; cell population; depletion; drug utilization; human; immunocompetent cell; mutation; non small cell lung cancer; nonhuman; oxidation; physical chemistry; Short Survey; treatment failjournal article10.1016/j.drudis.2021.07.014343250102-s2.0-85111913433https://scholars.lib.ntu.edu.tw/handle/123456789/579055