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article · Alexandria Dental Journal

BACTERIAL MICROBIOTA DYSBIOSIS: A NOVEL APPROACH ELUCIDATING ORAL CANCER

2025Open accessAlexandria University

Abstract

Introduction: The oral cavity contains a highly intricate microbial ecosystem that significantly contributes to the host's homeostasis. Emerging evidence suggests a critical role of the oral microbiome dysbiosis in Oral squamous cell carcinoma (OSCC) pathogenesis, with several oral pathogens being key prooncogenic bacteria. Objectives: Investigate the key differentially expressed genes (DEGs) and enriched pathways dysregulated in relation to Fusobacterium nucleatum and Streptococcus gordonii and their correlation with OSCCC using bioinformatics analysis. Material and Methods: Microarray dataset was processed and analyzed to obtain the DEGs in F. nucleatum and S. gordonii infected gingival cells, each compared to the control group. Enrichment pathway analysis of the identified DEGs from both analyses was done followed by their Protein- protein interaction network, identification of the hub genes of each analysis and their correlation with OSCC. Results: A total of 24 DEGs were identified in F. nucleatum infected keratinocytes with The most enriched KEGG terms include cancer pathways, Toll-like receptor signaling pathways and parathyroid hormone synthesis, secretion and action. The hub gene sequence is FOS, EGR1, NR4A2, GADD45B and FN1.Differential analysis of S. gordonii infected keratinocytes resulted in 30 DEGs with the most enriched KEGG terms involving MAPK signaling pathway and multiple cancers. The hub genes are EGR1, FOS, ATF3, MYC and RHOB. FOS and EGR1 were detected in common between the two analyses. These genes are strongly related to carcinogenesis and immune responses. Conclusion: Members of the oral microbiome may actively promote OSCC development and activate the expression of important factors linked to carcinogenesis.

Research topics

  • Oral Health Pathology and Treatment

Sustainable Development Goals

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DOI: 10.21608/adjalexu.2025.373917.1616

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