癌干细胞（CSCs）是一种具有自我更新能力和肿瘤启动性质的癌细胞子集。与其他非干细胞癌细胞不同，CSCs抵抗传统治疗，并仍然是疾病复发的主要原因之一。随着代谢组学的最新进展，各种研究表明CSCs具有独特的代谢特性。CSCs中的代谢重编程有助于自我更新和干性维持。越来越多的证据表明，能量代谢的重构是一个关键因素，它使得CSCs能够满足能量需求，维持干性并支持癌症的生长和侵袭。CSCs使用各种机制，例如增加糖酵解、氧化还原信号和自噬调节来克服营养缺乏并维持细胞生存。 CSCs所获得的脂质代谢改变，通过增加对脂肪酸合成和β氧化的依赖来支持生物量生产，并促进癌基因信号通路的贡献。本文综述了我们对CSCs中脂质代谢的当前理解，以及药物调节自噬和脂质代谢如何影响CSC表型。增加对脂质代谢的依赖似乎是一种吸引人的策略，可以使用专门针对调节脂质代谢的CSC的治疗剂来清除CSCs。 版权所有©2023 Elsevier Inc。

Cancer stem cells (CSCs) are a subset of cancer cells with self-renewal ability and tumor initiating properties. Unlike the other non-stem cancer cells, CSCs resist traditional therapy and remain a major cause of disease relapse. With the recent advances in metabolomics, various studies have demonstrated that CSCs have distinct metabolic properties. Metabolic reprogramming in CSCs contributes to self-renewal and maintenance of stemness. Accumulating evidence suggests that rewiring of energy metabolism is a key player that enables to meet energy demands, maintains stemness, and sustains cancer growth and invasion. CSCs use various mechanisms such as increased glycolysis, redox signaling and autophagy modulation to overcome nutritional deficiency and sustain cell survival. The alterations in lipid metabolism acquired by the CSCs support biomass production through increased dependence on fatty acid synthesis and β-oxidation and contribute to oncogenic signaling pathways. This review summarizes our current understanding of lipid metabolism in CSCs and how pharmacological regulation of autophagy and lipid metabolism influences CSC phenotype. Increased dependence on lipid metabolism appears as an attractive strategy to eliminate CSCs using therapeutic agents that specifically target CSCs based on their modulation of lipid metabolism.Copyright © 2023 Elsevier Inc. All rights reserved.