A substantial body of evidence has elucidated the critical role of gut microbiota in the development and progression of colorectal cancer (CRC). Gut dysbiosis, defined as the disruption of microbiome homeostasis, has been implicated in the pathogenesis of various diseases, including CRC, Parkinson’s disease, and autoimmune liver disorders. In recent years, research has increasingly focused on microbial metabolites, with numerous studies confirming their association with CRC. This review systematically elucidates the dual roles of microbial metabolites in the initiation and progression of CRC: they can suppress tumors by strengthening the gut barrier, reducing inflammation, blocking abnormal cell growth, and triggering apoptosis; yet under dysbiotic conditions-like chronic inflammation or epithelial injury-they may promote cancer by releasing inflammatory cytokines, damaging DNA, and driving uncontrolled proliferation. We summarize key findings on these metabolites’ functions in CRC, highlight emerging metabolite-targeted therapies, and identify major hurdles to clinical translation: metabolite instability, individual variation in host-microbe interactions, and absent biomarkers for patient selection. Because the gut microbiota-metabolite axis is central to CRC biology, targeting it rationally offers a promising path to more precise and effective treatments. Ultimately, gut metabolites are not just disease indicators-they are actionable therapeutic targets.
Jin et al. (Thu,) studied this question.
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