Lipids are a complex class of biomolecules with pivotal roles in the onset, progression, and maintenance of cancers. Lipids, derived from the tumor microenvironment (TME) or synthesized by cancer cells themselves, govern a large variety of pro-tumorigenic functions. In recent years, lipid metabolism and the reprogramming of liver cancer cells have received increasing attention, revealing that altered regulation of diverse lipid species, including triacylglycerols, phospholipids, sphingolipids, ceramides, fatty acids, and cholesterol, actively contributes to the initiation and progression of primary liver cancer. Lipid metabolic reprogramming also modifies the TME by influencing the recruitment, activation, and function of immune cells. Tumor-associated macrophages (TAM) are essential components of TME that sustain cancer growth, promoting invasion and mediating immune evasion. Macrophage polarization toward a tumor-supportive phenotype is associated with metabolic reprogramming. Indeed, lipid accumulation and enhanced fatty acid oxidation in TAM contribute to polarization to a M2 phenotype. In this review, we examine lipid metabolism in hepatocellular carcinoma and cholangiocarcinoma, focusing on TAM lipid metabolic reprogramming.
脂质是一类复杂的生物分子，在癌症的发生、进展及维持过程中发挥着关键作用。这些来源于肿瘤微环境或由癌细胞自身合成的脂质，调控着多种促肿瘤生成功能。近年来，脂质代谢与肝癌细胞的重编程日益受到关注，研究表明包括三酰甘油、磷脂、鞘脂、神经酰胺、脂肪酸及胆固醇在内的多种脂质分子的调控改变，在原发性肝癌的发生发展中起着重要作用。脂质代谢重编程还通过影响免疫细胞的募集、活化及功能改变肿瘤微环境。肿瘤相关巨噬细胞作为肿瘤微环境的核心组分，能够维持肿瘤生长、促进侵袭并介导免疫逃逸。巨噬细胞向促肿瘤表型的极化与代谢重编程密切相关。事实上，肿瘤相关巨噬细胞中的脂质积累和脂肪酸氧化增强会促进其向M2表型极化。本综述将探讨肝细胞癌和胆管癌中的脂质代谢，重点关注肿瘤相关巨噬细胞的脂质代谢重编程。
肿瘤(癌症)患者之家