Li Siqi, Yuan Hang, Li Liang, Li Qin, Lin Ping, Li Kai
Division of Abdominal Tumor Multimodality Treatment, Cancer Center and Lab of Experimental Oncology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.
Antioxidants (Basel). 2025 Feb 10;14(2):201. doi: 10.3390/antiox14020201.
Oxidative stress is a common event involved in cancer pathophysiology, frequently accompanied by unique lipid metabolic reprogramming phenomena. Oxidative stress is caused mainly by an imbalance between the production of reactive oxygen species (ROS) and the antioxidant system in cancer cells. Emerging evidence has reported that oxidative stress regulates the expression and activity of lipid metabolism-related enzymes, leading to the alteration of cellular lipid metabolism; this involves a significant increase in fatty acid synthesis and a shift in the way in which lipids are taken up and utilized. The dysregulation of lipid metabolism provides abundant intermediates to synthesize biological macromolecules for the rapid proliferation of cancer cells; moreover, it contributes to the maintenance of intracellular redox homeostasis by producing a variety of reducing agents. Moreover, lipid derivatives and metabolites play critical roles in signal transduction within cancer cells and in the tumor microenvironment that evades immune destruction and facilitates tumor invasion and metastasis. These findings suggest a close relationship between oxidative stress and lipid metabolism during the malignant progression of cancers. This review focuses on the crosstalk between the redox system and lipid metabolic reprogramming, which provides an in-depth insight into the modulation of ROS on lipid metabolic reprogramming in cancers and discusses potential strategies for targeting lipid metabolism for cancer therapy.
氧化应激是癌症病理生理学中常见的现象,常伴有独特的脂质代谢重编程现象。氧化应激主要由癌细胞中活性氧(ROS)产生与抗氧化系统之间的失衡引起。新出现的证据表明,氧化应激调节脂质代谢相关酶的表达和活性,导致细胞脂质代谢改变;这包括脂肪酸合成显著增加以及脂质摄取和利用方式的转变。脂质代谢失调为癌细胞的快速增殖提供了丰富的中间体以合成生物大分子;此外,它通过产生多种还原剂有助于维持细胞内氧化还原稳态。此外,脂质衍生物和代谢产物在癌细胞内以及肿瘤微环境中的信号转导中发挥关键作用,可逃避免疫破坏并促进肿瘤侵袭和转移。这些发现表明在癌症的恶性进展过程中氧化应激与脂质代谢之间存在密切关系。本综述聚焦于氧化还原系统与脂质代谢重编程之间的相互作用,深入探讨了ROS对癌症中脂质代谢重编程的调节作用,并讨论了针对脂质代谢进行癌症治疗的潜在策略。