• Microbiota modulate metastasis via immune regulation and EMT pathways. • Dysbiosis fosters systemic inflammation, aiding tumor dissemination. • Microbial metabolites influence the angiogenesis and immune evasion. • Pre-metastatic niches form via neutrophil traps and ECM remodeling. • Targeting the microbiome may enhance cancer therapy outcomes. The human microbiome has a significant influence on cancer metastasis through various mechanisms, including immune modulation, epithelial-mesenchymal transition, and the production of microbial metabolites. Dysbiosis alters intestinal homeostasis, facilitating systemic inflammation and creating pre-metastatic niches that support tumor dissemination. Specific microbial species, such as Fusobacterium nucleatum and Escherichia coli , have been identified as active participants in promoting metastatic pathways through the production of genotoxins and modulation of immune suppression. These microbes influence critical signaling cascades such as the Wnt/β-catenin, TGF-β, and NF-κB pathways, enabling tumor cells to evade immune surveillance and invade distant tissues. Microbial-derived pro-metastatic metabolites like trimethylamine N-oxide enhance angiogenesis and immune evasion. At the same time, short-chain fatty acids, such as butyrate and propionate, inhibit metastatic progression by suppressing histone deacetylation and promoting anti-inflammatory responses. The microbiome also influences pre-metastatic niche formation through neutrophil extracellular traps and extracellular matrix remodeling. Emerging evidence suggests that targeting the microbiome could enhance cancer therapy outcomes, particularly for metastatic cancers. This review comprehensively analyzes how microbiota contribute to metastasis and explores their therapeutic potential in precision oncology.
Islam et al. (2026) studied this question.