Gut microbiota as a mediator of cancer development and management: From colitis to colitis-associated dysplasia and carcinoma

Abstract

Colitis-associated colorectal cancer (CAC) develops as a result of prolonged colitis in patients with inflammatory bowel disease. In recent years, the role of the gut microbiota in colitis-associated colorectal carcinogenesis has begun to be recognized. Specific microbes, such as enterotoxigenic Bacteroides fragilis, Fusobacterium nucleatum, and pks⁺ Escherichia coli, promote carcinogenesis by regulating oncogenic signaling, epithelial-mesenchymal transition, autophagy induction, and the immune microenvironment. Conversely, commensal fungi and probiotics exert tumor-suppressive effects by inhibiting inflammatory pathways and immune cell recruitment. Emerging microbiota-targeted strategies, including precision probiotics and fecal microbiota transplantation, can restore ecological homeostasis, attenuate inflammation, and enhance the efficacy of conventional therapies. This review summarizes the current understanding of the mechanisms underlying microbiota-driven CAC pathogenesis and assesses the potential applications of gut microbiota in the development of diagnostic tools and therapeutic interventions.