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CancerGenetics

• When Bacterial Redox Meets Tumor Metabolism: Decoding the Enterococcus faecalis–Cancer Crosstalk

• Hanieh Safarzadeh,¹ Mohsen Moghoofei,^2,*
  1. Department of Microbiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
  2. Department of Virology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
  
  
  
• Introduction: The metabolic landscape of cancer is increasingly recognized as a dynamic ecosystem shaped not only by malignant cells but also by metabolically active microorganisms residing within or surrounding tumors. While several bacteria have been associated with cancer development, the metabolic mechanisms underlying these interactions remain incompletely understood. Enterococcus faecalis, an opportunistic Gram-positive bacterium capable of persistent intestinal colonization, represents a particularly intriguing candidate because of its capacity to generate extracellular superoxide and modulate the redox environment of host tissues. Rather than acting solely through conventional inflammatory pathways, E. faecalis may participate in cancer-associated metabolic crosstalk by altering oxidative metabolism, redox homeostasis, and host-cell stress responses. This review examines the emerging concept of E. faecalis as a metabolically active contributor to the tumor microenvironment, with emphasis on redox-mediated interactions and colorectal carcinogenesis.
• Methods: A narrative review was conducted using PubMed, Web of Science, and Scopus. Literature was identified using combinations of Enterococcus faecalis, colorectal cancer, cancer metabolism, bacterial metabolism, extracellular superoxide, oxidative stress, reactive oxygen species, redox homeostasis, DNA damage, tumor microenvironment, and microbial–host metabolic interaction. Mechanistic studies, experimental models, clinical investigations, and recent reviews were evaluated, with emphasis on evidence connecting bacterial metabolic activity to host-cell metabolic and molecular alterations.
• Results: Available evidence suggests that E. faecalis possesses metabolic characteristics capable of modifying the oxidative environment of host tissues. A particularly important feature is extracellular superoxide production, which can increase oxidative stress and potentially generate downstream reactive oxygen species capable of damaging cellular macromolecules. In the intestinal environment, persistent exposure to these bacterial-derived oxidants may interact with epithelial redox pathways and contribute to DNA damage and genomic instability, providing a mechanistic link between bacterial metabolism and tumor-promoting cellular phenotypes. Importantly, this interaction may extend beyond direct genotoxicity. Redox imbalance can alter mitochondrial function, cellular energy metabolism, antioxidant responses, and signaling pathways controlling proliferation and survival. E. faecalis may therefore participate in a metabolic feedback loop in which bacterial oxidative activity modifies host-cell metabolism, while the altered tumor microenvironment subsequently creates ecological conditions favorable for microbial persistence. Such interactions could be particularly relevant in colorectal cancer, where the intestinal microbiota, epithelial metabolism, inflammation, and oxygen gradients are closely interconnected. However, current evidence does not establish that E. faecalis independently causes cancer in humans. Its effects are likely influenced by bacterial strain, colonization density, microbial community composition, host genetics, diet, and inflammatory status. Consequently, the most plausible model is not a simple bacterium-to-cancer pathway but a redox-driven metabolic interaction network between bacterial metabolism, epithelial cells, immune cells, and the tumor microenvironment.
• Conclusion: Enterococcus faecalis provides a compelling model for investigating the emerging concept of bacterial redox metabolism as a component of cancer biology. Its capacity for extracellular superoxide production suggests a mechanistic interface between microbial metabolism, oxidative stress, DNA damage, and host metabolic reprogramming. Future studies combining spatial microbiology, bacterial metabolomics, redox profiling, and single-cell metabolic analysis could determine whether E. faecalis-associated metabolic signatures represent biomarkers of tumor progression or actionable therapeutic vulnerabilities. Understanding this metabolic crosstalk may ultimately shift the perspective of cancer-associated bacteria from passive biomarkers toward active metabolic participants in tumor ecology.
• Keywords: Enterococcus faecalis; cancer metabolism; colorectal cancer; bacterial metabolism; redox metabolism