ArticleInternational journal of oral science2025
Host-microbe computational proteomic landscape in oral cancer revealed key functional and metabolic pathways between Fusobacterium nucleatum and cancer progression.
Article in International journal of oral science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Porphyromonas gingivalis promotes oral squamous cell carcinoma progression via the IL-6/EZH2/Snai2 axis.Scientific reports · 2026Article
- Microbiota in cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- The tryptanthrin derivative g2 suppresses tongue squamous cell carcinoma via PI3K/AKT/P53 cathway modulation: evidence fromFrontiers in pharmacology · 2026Article
- Metabolic crosstalk between oral microbiota and the host in OSCC: emerging roles of microbial metabolites in tumor initiation and progression.Frontiers in cellular and infection microbiology · 2026Review
- Bacteriome-based oral dysbiosis index in patients with oral squamous cell carcinoma.Journal of oral microbiology · 2026Article
- Article
- Understanding the potential of probiotics in oral cancer prevention: a short review on microbial modulation.Discover oncology · 2025Review
- Microbial oncogenesis: the impact of Fusobacterium nucleatum on oral cancer pathways.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Fusobacterium in the microbiome: from health to disease across the oral-gut axis and beyond.NPJ biofilms and microbiomes · 2025Review
- The microbiome in cancer.iMeta · 2025Review
- Matrix Dynamics and Microbiome Crosstalk: Matrix Metalloproteinases as Key Players in Disease and Therapy.International journal of molecular sciences · 2025Review
- Article
- Machine learning models diagnose oral squamous cell carcinoma based on cross-cohort oral microbial signatures.Frontiers in microbiology · 2025Article
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24 authors.
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Abstract
Oral squamous cell carcinoma (OSCC) is the most common manifestation of oral cancer. It has been proposed that periodontal pathogens contribute to OSCC progression, mainly by their virulence factors. However, the main periodontal pathogen and its mechanism to modulate OSCC cells remains not fully understood. In this study we investigate the main host-pathogen pathways in OSCC by computational proteomics and the mechanism behind cancer progression by the oral microbiome. The main host-pathogen pathways were analyzed in the secretome of biopsies from patients with OSCC and healthy controls by mass spectrometry. Then, functional assays were performed to evaluate the host-pathogen pathways highlighted in oral cancer. Host proteins associated with LPS response, cell migration/adhesion, and metabolism of amino acids were significantly upregulated in the human cancer proteome, whereas the complement cascade was downregulated in malignant samples. Then, the microbiome analysis revealed large number and variety of peptides from Fusobacterium nucleatum (F. nucleatum) in OSCC samples, from which several enzymes from the L-glutamate degradation pathway were found, indicating that L-glutamate from cancer cells is used as an energy source, and catabolized into butyrate by the bacteria. In fact, we observed that F. nucleatum modulates the cystine/glutamate antiporter in an OSCC cell line by increasing SLC7A11 expression, promoting L-glutamate efflux and favoring bacterial infection. Finally, our results showed that F. nucleatum and its metabolic derivates promote tumor spheroids growth, spheroids-derived cell detachment, epithelial-mesenchymal transition and Galectin-9 upregulation. Altogether, F. nucleatum promotes pro-tumoral mechanism in oral cancer.
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