Research progress on oral microbiome in oral squamous cell carcinoma
10.12016/j.issn.2096-1456.202550478
- Author:
GONG Jiajing
1
;
LI Bo
2
;
LI Longjiang
1
Author Information
1. State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Department of Head and Neck Oncology, West China Hospital of Stomatology, Sichuan University
2. State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China Hospital of Stomatology, Sichuan University
- Publication Type:Review
- Keywords:
oral microbiome;
oral squamous cell carcinoma;
tumor microenvironment;
tumor immunology;
epigenetic;
bacterial;
Fusobacterium nucleatum;
Porphyromonas gingivalis;
virus;
epithelial-mesenchymal tran⁃sition;
histone acetylation;
NF-κB signaling pathway
- From:
Journal of Prevention and Treatment for Stomatological Diseases
2026;34(2):168-179
- CountryChina
- Language:Chinese
-
Abstract:
The homeostasis of the oral microbiome is essential for maintaining host health, and its disruption can contribute to the development of both oral and systemic diseases. The oral microbiome influences the initiation and progression of oral squamous cell carcinoma (OSCC) through multiple mechanisms. ① Oral microbes can directly act on epithelial cells, inducing cell-cycle dysregulation, DNA damage, and epigenetic reprogramming, thereby promoting cell proliferation and epithelial-mesenchymal transition (EMT). For example, Fusobacterium nucleatum binds to E-cadherin via its adhesin FadA, activating the β-catenin pathway and directly driving tumor-cell proliferation and EMT, while Porphyromonas gingivalis reprograms lipid synthesis to enhance the stemness of OSCC cells. ② Oral microbes and their metabolites reshape the tumor immune-suppressive microenvironment by altering the density, composition, and function of infiltrating immune cells. Periodontal pathogens induce a chronic inflammatory state in the oral cavity and activate signaling cascades such as MAPK/ERK and NF-κB, thereby indirectly accelerating OSCC progression. ③ Bacteria and viruses in the oral cavity exhibit synergistic interactions. Bacterial biofilms and proteases facilitate viral activation and infection, and microbial metabolites such as butyrate can enhance histone acetylation to promote the lytic reactivation of latent viruses. ④ At the ecological level, the depletion of commensals and expansion of anaerobic pathogens disrupt the metabolic network of the community, and complex interspecies interactions collectively shape a pro-carcinogenic niche that drives OSCC progression on multiple fronts. Future studies should integrate multi-omics analyses with longitudinal clinical cohorts to explore functional causal networks of key microbial communities and develop individualized targeted intervention strategies for microecology.
- Full text:2026020511152862328口腔微生物组在口腔鳞状细胞癌中的研究进展.pdf
