The diet-microbiota-inflammation axis and colorectal cancer

Area of Science:

• Gastroenterology
• Oncology
• Microbiology

Background:

• Colorectal cancer (CRC) remains a major global health concern.
• Diet, gut microbiota, microbial metabolites, and chronic inflammation are increasingly recognized as key factors in colorectal carcinogenesis.
• These factors present novel opportunities for CRC prevention, diagnosis, and treatment.

Purpose of the Study:

• To comprehensively review the current evidence on the role of diet, nutrition, microbial metabolism, and chronic inflammation in CRC.
• To emphasize emerging translational applications, including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.

Main Methods:

• A systematic literature search was conducted using PubMed, Scopus, and the Cochrane Library.
• Relevant studies focusing on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were reviewed.
• Preclinical studies, clinical studies, high-quality reviews, and meta-analyses were considered.

Main Results:

• Diet profoundly impacts gut microbiota composition and function; high-fiber diets and short-chain fatty acids (SCFAs) appear protective against CRC.
• Western diets, ultra-processed foods, and dysbiosis-associated metabolites promote a pro-inflammatory environment linked to carcinogenesis.
• Specific microorganisms like *Fusobacterium nucleatum* are associated with CRC through inflammatory and genotoxic mechanisms.
• Advances in multi-omics and sequencing technologies enable the identification of microbial signatures for diagnosis and prognosis.
• Microbiota-targeted interventions (probiotics, prebiotics, FMT) show promising preclinical and early clinical results.

Conclusions:

• The diet-microbiota-inflammation axis is central to colorectal carcinogenesis and a promising area for translational research.
• Microbiome-based biomarkers and microbiota-targeted therapies hold potential for precision prevention and personalized CRC management.
• Challenges remain in establishing causation, standardization, and clinical translation of these findings.