Understanding the characteristics of the host genome and microbiome interaction in oral squamous cell carcinoma: a narrative review
Background Oral health status is directly associated with microbes present within it. The abundance of microbes at the OSCC site is more than at its control site, representing its possible role in the progression of OSCC development. Dysbiosis of oral microbiota could be a crucial etiological risk f...
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Veröffentlicht in: | Beni-Suef University journal of basic and applied sciences 2022-10, Vol.11 (1), p.1-8, Article 126 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Background
Oral health status is directly associated with microbes present within it. The abundance of microbes at the OSCC site is more than at its control site, representing its possible role in the progression of OSCC development. Dysbiosis of oral microbiota could be a crucial etiological risk factor in the elevation of OSCC. This study aimed to analyze and assess: a) positive regulator microbes of oral cancer and their abundance at the cancer site, b) pathways involved in positive regulator microbes, and c) identification of the most virulent oral oncogenic microbe.
Main body
It is obtained from several studies that microbes belonging to
Prevotella, Fusobacterium, Alloprevotella, Capnocytophaga, Porphyromonas, Campylobacter, and Aggregatibacter
are detected to be more in number contrast to healthy site
s. Fusobacterium nucleatum, Porphyromonas gingivalis, and Candida albicans
show molecular pathways linked with OSCC development. Genes encoding for virulent factors like FimA, Gingipains, lipopolysaccharide (
P. gingivalis)
, FadA, Fap2 (
F. nucleatum
), and zymosan (
C. Albicans
) are directly involved in elevating oral cancer.
Conclusion
Mostly, the genes that are involved in promoting oral cancer are the genes that generally encode cell wall proteins. The cell wall proteins that is FadA, Fap, and FimA interact with the host's cell and hamper the normal regulation pathway, which leads to activation of cell proliferating pathways, down-regulates apoptotic pathways, cytoskeleton rearrangement, and upregulates the cell cycle checkpoint regulators; as a result, progression of oral cancer occurs. |
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ISSN: | 2314-8543 2314-8543 |
DOI: | 10.1186/s43088-022-00306-z |