College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam 13488, Korea.
College of Pharmacy, Keimyung University, Daegu 42601, Korea.
Int J Mol Sci. 2021 Apr 22;22(9):4376. doi: 10.3390/ijms22094376.
The nuclear factor-erythroid 2 p45-related factor 2 (NRF2, also called ) and its cytoplasmic repressor, Kelch-like ECH-associated protein 1 (KEAP1), are major regulators of redox homeostasis controlling a multiple of genes for detoxification and cytoprotective enzymes. The NRF2/KEAP1 pathway is a fundamental signaling cascade responsible for the resistance of metabolic, oxidative stress, inflammation, and anticancer effects. Interestingly, a recent accumulation of evidence has indicated that NRF2 exhibits an aberrant activation in cancer. Evidence has shown that the NRF2/KEAP1 signaling pathway is associated with the proliferation of cancer cells and tumerigenesis through metabolic reprogramming. In this review, we provide an overview of the regulatory molecular mechanism of the NRF2/KEAP1 pathway against metabolic reprogramming in cancer, suggesting that the regulation of NRF2/KEAP1 axis might approach as a novel therapeutic strategy for cancers.
核因子红细胞 2 p45 相关因子 2（NRF2，也称为 ）及其细胞质抑制剂，Kelch 样 ECH 相关蛋白 1（KEAP1），是调节氧化还原平衡的主要调节剂，控制多种解毒和细胞保护酶的基因。NRF2/KEAP1 途径是一种基本的信号级联反应，负责抵抗代谢、氧化应激、炎症和抗癌作用。有趣的是，最近越来越多的证据表明 NRF2 在癌症中表现出异常激活。有证据表明，NRF2/KEAP1 信号通路通过代谢重编程与癌细胞的增殖和肿瘤发生有关。在这篇综述中，我们概述了 NRF2/KEAP1 通路对癌症代谢重编程的调节分子机制，表明 NRF2/KEAP1 轴的调节可能成为癌症的一种新的治疗策略。
