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Review
. 2023 Oct 26:14:1198269.
doi: 10.3389/fimmu.2023.1198269. eCollection 2023.

The emerging role of oral microbiota in oral cancer initiation, progression and stemness

Affiliations
Review

The emerging role of oral microbiota in oral cancer initiation, progression and stemness

Partha Jyoti Saikia et al. Front Immunol. .

Abstract

Oral squamous cell carcinoma (OSCC) is the most prevalent malignancy among the Head and Neck cancer. OSCCs are highly inflammatory, immune-suppressive, and aggressive tumors. Recent sequencing based studies demonstrated the involvement of different oral microbiota in oral cavity diseases leading OSCC carcinogenesis, initiation and progression. Researches showed that oral microbiota can activate different inflammatory pathways and cancer stem cells (CSCs) associated stemness pathways for tumor progression. We speculate that CSCs and their niche cells may interact with the microbiotas to promote tumor progression and stemness. Certain oral microbiotas are reported to be involved in dysbiosis, pre-cancerous lesions, and OSCC development. Identification of these specific microbiota including Human papillomavirus (HPV), Porphyromonas gingivalis (PG), and Fusobacterium nucleatum (FN) provides us with a new opportunity to study the bacteria/stem cell, as well as bacteria/OSCC cells interaction that promote OSCC initiation, progression and stemness. Importantly, these evidences enabled us to develop in-vitro and in-vivo models to study microbiota interaction with stem cell niche defense as well as CSC niche defense. Thus in this review, the role of oral microbiota in OSCC has been explored with a special focus on how oral microbiota induces OSCC initiation and stemness by modulating the oral mucosal stem cell and CSC niche defense.

Keywords: altruistic stem cells (ASCs); cancer stem cells (CSCs); epithelial mesenchymal transition (EMT); oral leukoplakia (OLK); oral squamous cell carcinoma (OSCC); stemness.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Potential activation of diverse cellular pathways in oral cancer cells by oral microbiota and bacterial metabolites.
Figure 2
Figure 2
Fusobacterium nucleatum (FN) induced tumor stemness switch of Non-CSCs to CSC. (A) CSCs interact with F. nucleatumand reprogram to tumor stemness defense (TSD) phenotype. The TSD phenotype enhances the expression of Fap2 and Fad A in FN. (B) The reprogrammed FN along with HPV-16 then reprograms Non Stem Cancer Cells (non-CSCs) to CSCS by inducing tumor stemness switch (88, 89).

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