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The FnBPA from methicillin-resistant Staphylococcus aureus promoted development of oral squamous cell carcinoma
BACKGROUND: Oral squamous cell carcinoma (OSCC) is the most common tumor in the oral cavity. Methicillin-resistant Staphylococcus aureus (MRSA) were highly detected in OSCC patients; however, the interactions and mechanisms between drug-resistant bacteria (MRSA) and OSCC are not clear. AIM: The aim...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9291692/ https://www.ncbi.nlm.nih.gov/pubmed/35859766 http://dx.doi.org/10.1080/20002297.2022.2098644 |
Sumario: | BACKGROUND: Oral squamous cell carcinoma (OSCC) is the most common tumor in the oral cavity. Methicillin-resistant Staphylococcus aureus (MRSA) were highly detected in OSCC patients; however, the interactions and mechanisms between drug-resistant bacteria (MRSA) and OSCC are not clear. AIM: The aim of this study was to investigate the promotion of MRSA on the development of OSCC. METHODS: MRSA and MSSA (methicillin-susceptible) strains were employed to investigate the effect on the proliferation of OSCC in vitro and vivo. RESULTS: All of the MRSA strains significantly increased the proliferation of OSCC cells and MRSA arrested the cell cycles of OSCC cells in the S phase. MRSA activated the expression of TLR-4, NF-κB and c-fos in OSCC cells. MRSA also promoted the development of squamous cell carcinoma in vivo. The virulence factor fnbpA gene was significantly upregulated in all MRSA strains. By neutralizing FnBPA, the promotions of MRSA on OSCC cell proliferation and development of squamous cell carcinoma were significantly decreased. Meanwhile, the activation of c-fos and NF-κB by MRSA was also significantly decreased by FnBPA antibody. CONCLUSION: MRSA promoted development of OSCC, and the FnBPA protein was the critical virulence factor. Targeting virulence factors is a new method to block the interaction between a drug-resistant pathogen and development of tumors. |
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