Exploring the Relationship Between Colitis-Associated Cancer and Lipid Metabolism Reprogramming from the Perspective of Inflammation-Cancer Transformation

Colitis-associated colorectal cancer (CAC) is the most severe complication of inflammatory bowel disease (IBD), characterized by multifocal lesions and poor prognosis. Aberrant lipid metabolism drives CAC progression by modulating the tumor microenvironment, activating oncogenic pathways, and facilitating immune escape. These metabolic alterations supply energy for tumor cells, disrupt the homeostasis of the tumor microenvironment, and contribute to gut microbiota dysbiosis, ultimately establishing a vicious cycle of “metabolism–inflammation–carcinogenesis.” Although the role of lipid metabolism in sporadic colorectal cancer has been extensively studied, the specific metabolic rewiring that triggers the malignant switch during chronic colitis remains systematically unexplored. From the viewpoint of the dynamic transition toward malignancy, this review dissects the synergistic interactions between lipid metabolism and inflammatory signaling, immune microenvironment remodeling, and intestinal dysbiosis during this evolutionary process. It systematically summarizes key genes and potential therapeutic targets governing lipid metabolism in CAC and investigates the translational value of targeting lipid metabolic reprogramming for early intervention and combination therapies in CAC. By integrating current evidence, this article clarifies how lipid reprogramming orchestrates the inflammation-to-cancer shift, providing novel research insights and therapeutic strategies to improve clinical prognosis for CAC patients.