By Ana Espino | Published on March 13, 2026 | 3 min readColorectal cancer (CRC) is among the
most common and most lethal cancers worldwide. While established risk
factors—diet, obesity, smoking, and physical inactivity—are well recognized,
they do not fully explain tumor initiation and progression. Scientific
attention has therefore increasingly turned to the
intestinal microbiota, a
central actor in digestive and immune homeostasis.
The gut microbiota modulates the
intestinal barrier, local inflammation, and the production of bioactive
metabolites.
Dysbiosis, characterized by an alteration in microbial diversity
and bacterial composition, may promote a pro-tumorigenic microenvironment.
However, the precise nature of the interactions between the microbiota and
colorectal epithelial cells remains complex and multifactorial.
This review, recently published in
the International Journal of Molecular Sciences, analyzes the mechanisms
by which the intestinal microbiota influences CRC initiation, progression, and
therapeutic response, highlighting the bacterial species involved and their
associated molecular pathways.
Do certain bacteria trigger cancer?
Patients with CRC often exhibit
reduced microbial diversity together with an expansion of pro-inflammatory and
potentially oncogenic bacteria. Among the most studied species are Fusobacterium
nucleatum, colibactin-producing Escherichia coli, and
enterotoxigenic Bacteroides fragilis.
Fusobacterium nucleatum promotes cellular adhesion,
activates the Wnt/β-catenin
signaling pathway, and stimulates tumor proliferation. Certain strains of E.
coli produce colibactin, a genotoxin that induces DNA double-strand breaks.
Bacteroides fragilis secretes a toxin capable of activating the NF-κB pathway, thereby amplifying
chronic inflammation.
At the same time, the reduction of
butyrate-producing bacteria—short-chain fatty acid producers with
anti-inflammatory and anti-proliferative properties—weakens epithelial
protection. This loss promotes increased intestinal permeability and sustained
immune activation.
The microbiota also influences the
tumor microenvironment and responses to treatment. Certain bacterial profiles
are associated with improved responses to chemotherapy or immunotherapy,
suggesting a potential prognostic and predictive role.
Restoring balance for prevention
Colorectal cancer results from
complex interactions between genetics, environment, and immunity. This review
aimed to clarify the role of the intestinal microbiota in colorectal
carcinogenesis.
The data indicate that certain
pro-inflammatory and genotoxic bacteria actively contribute to tumor
initiation, while the loss of protective species promotes an environment
conducive to disease progression. The microbiota therefore appears to act as a
dynamic cofactor in tumorigenesis and may also influence therapeutic response.
However, most available data remain
observational. Establishing causality and ensuring interindividual
reproducibility will require robust, standardized longitudinal studies.
In the longer term, identifying
specific microbial signatures, developing targeted modulation strategies—such
as probiotics, prebiotics, or fecal microbiota transplantation—and integrating
microbiota analysis into screening algorithms could transform the prevention
and management of colorectal cancer.
Read next: Colorectal cancer: mRNA nanobodies open a new avenue in immunotherapy
About the author – Ana EspinoPhD 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.
