Research advances in inflammation-driven mechanisms of colorectal cancer evolution

SU Jingyue; NI Xuefeng

doi:10.3969/j.issn.1009-0460.2026.01.015

Abstract：Inflammation is considered a key driver of the initiation and progression of colorectal cancer.During the initial stage of colorectal cancer,risk factors such as inflammatory bowel disease,dysbiosis of the gut microbiota,and metabolic abnormalities promote the accumulation of driver gene mutations and the clonal expansion of mutated epithelial cells by inducing oxidative stress,disruption of the intestinal barrier,and abnormal immune responses,thereby triggering early events in the transition from inflammation to cancer.In the progression stage,tumor cells,immune cells,stromal cells,and intratumoral microorganisms together form a self-sustaining inflammatory tumor microenvironment,driving immunosuppression,angiogenesis,and stromal remodeling,thereby endowing the tumor with sustained proliferation and invasive capabilities.During the establishment of the pre-metastatic microenvironment,remote signals such as exosomes and intratumoral bacteria released from the primary tumor,combined with the anatomical features of portal venous drainage in colorectal cancer and the liver's inherent susceptibility to inflammation and immune tolerance,collectively promote the formation of a pre-metastatic niche that facilitates the dissemination,colonization,and growth of tumor cells.Finally,this article summarizes preliminary evidence supporting anti-inflammatory therapeutic strategies in colorectal cancer.In the future,an integrated intervention system centered on inflammation regulation and combined with immunotherapy and targeted therapies will provide new insights and targets for the precise prevention and treatment of colorectal cancer.