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Войти в исследования Biochemical and biophysical research communications · 2026
Supernatants from DNase-deficient Prevotella intermedia strains enhance oral squamous cell carcinoma cell migration and invasion by activating inflammatory and epithelial-mesenchymal transition pathways.
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Seto-Tetsuo Fumi, Katase Naoki, Sasaki Yuko, Yukitake Hideharu, Naito Mariko
Аннотация
INTRODUCTIONS: Oral squamous cell carcinoma (OSCC) has been increasingly associated with dysbiosis of the oral microbiome. Among oral pathogens, Prevotella intermedia (P. intermedia) is frequently enriched in patients with OSCC; however, the role of its virulence factors-particularly its deoxyribonuclease (DNase) activity-remains poorly understood.
METHODS: We compared the effects of culture supernatants from wild-type P. intermedia OMA14 and DNase-deficient mutant strains (nucA, nucD and nucA nucD) on the migration and invasion of the OSCC cell line SAS, using wound healing and Matrigel invasion assays. Transcriptomic profiling of SAS cells exposed to bacterial supernatants was performed using RNA sequencing (RNA-seq), followed by differential gene expression and pathway enrichment analyses.
RESULTS: Supernatants from the nucA nucD mutant strain significantly enhanced SAS cells migration and invasion compared with those from the OMA14 strain. RNA-seq revealed marked transcriptomic reprogramming, including upregulation of genes related to extracellular matrix degradation, epithelial-mesenchymal transition (EMT), and inflammatory signaling. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses confirmed the enrichment of EMT, cytokine signaling, and tumor-promoting pathways.
CONCLUSIONS: Our findings demonstrate a dual role of bacterial DNase activity in SAS cell. Although DNases contribute to immune evasion via neutrophil extracellular trap degradation, their absence enhances tumor invasion by promoting proinflammatory and EMT-related transcriptional programs. These results highlight the complex interplay between microbial nucleases, extracellular DNA, and host signaling, providing novel insights into the contribution of the oral microbiome to OSCC pathogenesis.
METHODS: We compared the effects of culture supernatants from wild-type P. intermedia OMA14 and DNase-deficient mutant strains (nucA, nucD and nucA nucD) on the migration and invasion of the OSCC cell line SAS, using wound healing and Matrigel invasion assays. Transcriptomic profiling of SAS cells exposed to bacterial supernatants was performed using RNA sequencing (RNA-seq), followed by differential gene expression and pathway enrichment analyses.
RESULTS: Supernatants from the nucA nucD mutant strain significantly enhanced SAS cells migration and invasion compared with those from the OMA14 strain. RNA-seq revealed marked transcriptomic reprogramming, including upregulation of genes related to extracellular matrix degradation, epithelial-mesenchymal transition (EMT), and inflammatory signaling. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses confirmed the enrichment of EMT, cytokine signaling, and tumor-promoting pathways.
CONCLUSIONS: Our findings demonstrate a dual role of bacterial DNase activity in SAS cell. Although DNases contribute to immune evasion via neutrophil extracellular trap degradation, their absence enhances tumor invasion by promoting proinflammatory and EMT-related transcriptional programs. These results highlight the complex interplay between microbial nucleases, extracellular DNA, and host signaling, providing novel insights into the contribution of the oral microbiome to OSCC pathogenesis.