Zhou Runkai, Wang Fazhi, Wen Jiazhe, Zhou Xuefeng, Wen Yugang
Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
School of Basic Medical Sciences, Fudan University, Shanghai, China.
Cancer Med. 2025 Sep;14(17):e71185. doi: 10.1002/cam4.71185.
Colorectal cancer (CRC) is one of the most common malignant tumors, and its morbidity ranks third among all cancers, with a trend toward younger patients. Metabolic reprogramming, a unique metabolic mode in tumor cells, is closely related to the occurrence and development of CRC. Numerous studies have confirmed that many genetic and protein changes can regulate cellular metabolic reprogramming, of which changes in glucose metabolism have the greatest impact. These aberrant metabolic processes provide energy and essential nutrients to CRC cells, promoting their proliferation and metastasis and influencing tumor resistance. The purpose of this review is to outline the role of glucose metabolic reprogramming in the onset and development of CRC, discuss the research progress in the dual reprogramming of glucose metabolism and lipid metabolism or glucose metabolism and amino acid metabolism, and address the issues of targeted metabolism therapy and drug resistance.
We searched PubMed for review articles published in English between January 1, 2015, and April 26, 2024, which included "Colorectal Neoplasms" with "Metabolic Reprogramming" OR "Glucose Metabolism Disorders" OR "The Warburg Effect" OR "Targeted Therapy." Subsequently, the literature was classified, organized, and summarized. Various types of studies were integrated and compiled into this review. Additionally, mechanism diagrams were drawn to facilitate the understanding of this study. The figures were created using BioRender.com and has obtained the official publication license.
Glucose metabolic reprogramming serves as a pivotal driver of CRC initiation, progression, and chemoresistance, while its crosstalk with lipid or amino acid metabolic reprogramming further amplifies the malignant phenotype of CRC. Targeted therapeutic strategies aiming at glucose metabolic reprogramming (such as metabolic inhibitors, combination with immunotherapy) and related clinical research have demonstrated potential for inhibiting CRC progression and improving treatment outcomes.
结直肠癌(CRC)是最常见的恶性肿瘤之一,其发病率在所有癌症中排名第三,且有患者年轻化的趋势。代谢重编程是肿瘤细胞中一种独特的代谢模式,与CRC的发生发展密切相关。大量研究证实,许多基因和蛋白质变化可调节细胞代谢重编程,其中葡萄糖代谢变化的影响最大。这些异常的代谢过程为CRC细胞提供能量和必需营养物质,促进其增殖和转移,并影响肿瘤耐药性。本综述的目的是概述葡萄糖代谢重编程在CRC发生发展中的作用,讨论葡萄糖代谢与脂质代谢或葡萄糖代谢与氨基酸代谢双重重编程的研究进展,并探讨靶向代谢治疗和耐药性问题。
我们在PubMed上检索了2015年1月1日至2024年4月26日期间发表的英文综述文章,检索词包括“结直肠肿瘤”与“代谢重编程”或“葡萄糖代谢紊乱”或“瓦伯格效应”或“靶向治疗”。随后,对文献进行分类、整理和总结。将各类研究进行整合并汇编成本综述。此外,绘制了机制图以方便理解本研究。这些图是使用BioRender.com创建的,并已获得官方出版许可。
葡萄糖代谢重编程是CRC起始、进展和化疗耐药的关键驱动因素,而其与脂质或氨基酸代谢重编程的相互作用进一步放大了CRC的恶性表型。针对葡萄糖代谢重编程的靶向治疗策略(如代谢抑制剂、与免疫疗法联合)及相关临床研究已显示出抑制CRC进展和改善治疗效果的潜力。