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