Colorectal cancer (CRC) is a leading cause of global cancer incidence and mortality, with rising prevalence among younger individuals. Accumulating evidence reveals a critical pathological axis linking intestinal barrier disruption, gut microbial dysbiosis, and chronic inflammation, collectively driving CRC initiation. Early colorectal lesions exhibit microbial shifts—reduced α-diversity with clear β-diversity separation, enrichment of oral-origin/pathobiont taxa and depletion of butyrate producers—alongside impaired mucus and tight junction integrity. Concurrent chemical barrier drifts, with decreased short-chain fatty acids and increased secondary bile acids, enhance epithelial stress and vulnerability. The resultant permeability facilitates the translocation of microbial products, triggering inflammation and tumorigenesis. This paper focuses on a review of the relationship between gut microbiota, intestinal barrier, inflammatory signaling pathways, and tumor initiation, sorting out its potential role in developing, diagnosing, and treating CRC. Collectively, this cascade axis offers theoretical and empirical support for the early pathological detection and intervention of CRC, indicating promising directions for future precision screening and stratified management strategies.
Dong et al. (2026) studied this question.