Microbiome and colorectal cancer: the invisible enemy?

By Ana Espino | Published on March 3rd, 2026 | 3 min read


Colorectal cancer (CRC) remains one of the most common and deadliest cancers worldwide. Despite the identification of classic risk factors—diet, obesity, smoking, and physical inactivity—a significant part of its pathophysiology is still not fully explained.  

The gut microbiota, made up of billions of microorganisms, plays a central role in digestive homeostasis, immune regulation, and metabolism. Intestinal dysbiosis—characterized by altered microbial diversity and composition—is now implicated in many inflammatory and metabolic diseases.  

However, the mechanisms linking dysbiosis and colorectal carcinogenesis remain complex. This recent review analyzes the interactions between the gut microbiota, chronic inflammation, and tumor transformation, detailing the bacterial species involved and the underlying molecular pathways.  

Can the microbiota initiate carcinogenesis?  

This narrative review synthesizes evidence from experimental, clinical, and metagenomic studies exploring the role of dysbiosis in CRC.  

Analyses show reduced bacterial diversity in CRC patients, associated with an expansion of pro-inflammatory species. Among the most studied bacteria are Fusobacterium nucleatum, colibactin-producing Escherichia coli, and enterotoxigenic Bacteroides fragilis.  

Fusobacterium nucleatum promotes cellular adhesion, activates β-catenin pathways, and stimulates tumor cell proliferation. Certain E. coli strains produce colibactin, a genotoxin capable of inducing DNA double-strand breaks. Bacteroides fragilis secretes a toxin that promotes chronic inflammation and activation of the NF-κB pathway.  

Dysbiosis also disrupts the production of short-chain fatty acids, especially butyrate, which is known for anti-inflammatory and anti-proliferative properties. Reduced levels of these protective metabolites contribute to increased intestinal permeability and chronic immune stimulation.  

Experimental data show that the microbiota modulates the tumor microenvironment, influences immune infiltration, and can alter responses to treatment, including immunotherapy. Certain microbial profiles are associated with better therapeutic responses, suggesting a potential prognostic role.  

Rebalancing to prevent?  

Colorectal cancer results from a complex interaction between genetic, environmental, and immune factors. This review aimed to clarify the specific contribution of intestinal dysbiosis to colorectal carcinogenesis.  

The evidence supports that certain pro-inflammatory and genotoxic bacteria actively contribute to tumor transformation, while the loss of beneficial bacteria weakens protective mechanisms. The microbiota therefore appears to be a central actor in the tumor microenvironment, capable of influencing initiation, progression, and treatment response.  

However, most studies remain observational or experimental. Establishing causality and accounting for inter-individual reproducibility will require more robust longitudinal investigations.  

Ultimately, identifying microbial biomarkers, developing targeted modulation strategies—probiotics, prebiotics, fecal microbiota transplantation—and integrating the microbiota into screening algorithms could transform the preventive and therapeutic approach to colorectal cancer.   

Read next: Colorectal cancer on the rise

About the author – Ana Espino
PhD in Immunology, specialized in Virology  
As a scientific writer, Ana is passionate about bridging the gap between research and real-world impact. With expertise in immunology, virology, oncology, and clinical studies, she makes complex science clear and accessible. Her mission: to accelerate knowledge sharing and empower evidence-based decisions through impactful communication.