引用文本：王瑞雪, 胡海清. 脂代谢重编程在结直肠癌发生发展中的作用及机制研究进展[J/CD]. 消化肿瘤杂志（电子版）, 2026, 18(3): 451-459.

作者：王瑞雪1，胡海清2

单位：1. 内蒙古医科大学附属肿瘤医院（北京大学肿瘤医院内蒙古医院），内蒙古自治区 呼和浩特 010000；2. 内蒙古医科大学附属肿瘤医院（北京大学肿瘤医院内蒙古医院） 内镜中心，内蒙古自治区 呼和浩特 010000

Authors：Wang Ruixue1, Hu Haiqing2

Unit：1. Affiliated Cancer Hospital of Inner Mongolia Medical University (Inner Mongolia Hospital, Peking University Cancer Hospital), Hohhot 010000, Inner Mongolia, China；2. Endoscopy Center, Affiliated Cancer Hospital of Inner Mongolia Medical University (Inner Mongolia Hospital, Peking University Cancer Hospital), Hohhot 010000, Inner Mongolia, China

摘要：

结直肠癌（colorectal cancer, CRC）是全球高发的消化系统恶性肿瘤，其发生发展不仅与经典基因突变相关，还伴随着显著的代谢重编程。近年研究表明，脂代谢异常是CRC进展的重要驱动因素。CRC细胞通过增强脂肪酸从头合成、脂质摄取、脂肪酸氧化及胆固醇代谢，满足自身快速增殖、侵袭转移及治疗适应的需求。同时，肿瘤相关脂肪细胞、免疫细胞及肠道菌群通过提供脂质底物并重塑免疫代谢状态，进一步强化脂代谢依赖。本文认为，CRC脂代谢重编程可被概括为一个多层级驱动系统，包括内在致癌信号介导的代谢编程、肿瘤微环境驱动的代谢强化以及适应性进化获益3个层面。该系统不仅支持肿瘤生长，还促进免疫逃逸、铁死亡抵抗及治疗耐受。此外，脂代谢相关分子在诊断分型及预后评估中展现出潜在价值，靶向脂代谢的联合治疗策略亦成为重要发展方向。然而，代谢补偿、肿瘤异质性及毒性问题仍限制其临床应用。未来研究需结合多组学与空间技术，解析脂代谢依赖的层级结构，从而推动精准干预策略的临床转化。

关键词：结直肠癌；脂代谢；代谢重编程；肿瘤微环境；靶向治疗

Abstract：

Colorectal cancer (CRC) is one of the most prevalent gastrointestinal malignancies worldwide. Its initiation and progression are not only associated with classical genetic mutations but also accompanied by pronounced metabolic reprogramming. In recent years, dysregulated lipid metabolism has been increasingly recognized as a key driver of CRC progression. CRC cells enhance de novo fatty acid synthesis, lipid uptake, fatty acid oxidation, and cholesterol metabolism to meet the demands of rapid proliferation, invasion, metastasis, and therapeutic adaptation. Meanwhile, tumor-associated adipocytes, immune cells, and the gut microbiota further reinforce lipid metabolic dependency by supplying lipid substrates and reshaping immune metabolic status. This review summarizes CRC lipid metabolic reprogramming as a multi-level driving system, including oncogenic signal-mediated metabolic programming, tumor microenvironment-driven metabolic reinforcement, and adaptive evolutionary advantages. This system not only supports tumor growth but also promotes immune evasion, ferroptosis resistance, and therapeutic tolerance. In addition, lipid metabolism-related molecules show potential value in diagnostic stratification and prognostic assessment, and combination strategies targeting lipid metabolism have emerged as important therapeutic directions. However, metabolic compensation, tumor heterogeneity, and toxicity remain major limitations for clinical application. Future studies integrating multi-omics and spatial technologies are needed to elucidate the hierarchical structure of lipid metabolic dependency and to facilitate the clinical translation of precision intervention strategies.

Key words：Colorectal cancer; Lipid metabolism; Metabolic reprogramming; Tumor microenvironment; Targeted therapy

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