溃疡性结肠癌(CAC)是一种特殊类型的结直肠癌，它主要发生于患有炎症性肠病(IBD)的人群，与长期慢性结肠炎相关。慢性炎症被认为是CAC发展和进展的最关键因素，炎症反应的程度和持续性是IBD患者CAC进展的主要驱动因素。细胞自噬/自噬是一种有助于维护肠黏膜屏障和调节肠道炎症的细胞过程，对于减缓IBD进展效果显著。然而，自噬障碍对CAC发病机制的确切贡献尚未完全阐明，尽管我们认为自噬通过调节肠道炎症和其他因素，可能降低CAC的风险。本综述总结了最近CAC发展的研究，并探究自噬在减少CAC发病中的可能功能。此外，我们还探讨了CAC转化后自噬的功能转换，并提出通过促进自噬来减缓CAC的发病，可能作为预防与IBD相关CAC的新策略。

Colitis-associated colon cancer (CAC) is a distinct form of colorectal cancer that emerges from prolonged colitis in individuals with inflammatory bowel disease (IBD). Chronic inflammation is considered as the most critical contributor to the development and progression of CAC, with the degree and persistence of the inflammatory response being the primary drivers of CAC progression in individuals with IBD. Macroautophagy/autophagy, which is a cellular process that aids in preserving the intestinal mucosal barrier and regulating intestinal inflammation, is effective in reducing IBD progression. However, the precise contribution of impaired autophagy to CAC pathogenesis has yet to be fully elucidated. Nevertheless, it is thought that autophagy may reduce the risk of CAC by regulating intestinal inflammation and other factors. This review summarizes recent research on CAC development and investigates the possible functions of autophagy in reducing CAC initiation. Furthermore, we explore the functional transformation of autophagy after CAC transformation and propose that promoting autophagy as a means of attenuating CAC initiation may serve as a novel strategy for preventing IBD-related CAC.