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Updated: Jul 7, 2026
Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Methicillin-resistant Staphylococcus aureus extracellular vesicles induced IL-8 dependent proliferation in oral
Yuke Shou1, Yangyang Shi1, Lixin Kong2
1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China; Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China.
Introduction:
The microbes within the tumor microenvironment are one of the important risk factors for tumor development, but the actions of antibiotic-resistant bacteria on the tumor development remain unclear. Methicillin-resistant Staphylococcus aureus (MRSA) is frequently detected in oral cavities of oral squamous cell carcinoma (OSCC) patients, especially after radiotherapy and/or chemotherapy, and is associated with adverse prognosis. However, the effects of MRSA on OSCC development are not clear.
Objectives:
This study aims to determine whether and how MRSA‑derived extracellular vesicles (EVs) affect OSCC proliferation and tumor development.
Methods:
EVs were isolated from MRSA and methicillin‑susceptible S. aureus (MSSA). Their effects on OSCC cells were evaluated by proliferation assays, EV internalization, protein cargo analysis, and signaling pathway inhibition. An ectopic tumor mouse model with IL‑8 knockout or CXCR1 blockade was used for in vivo validation.
Results:
Nano-size EVs derived from MRSA, compared with those from MSSA, could enter OSCC cells and promote cell proliferation and tumor development, while the proteins were the most important cargos. Mechanistically, MRSA EVs activated ERK/c‑Jun signaling pathway to produce the chemokine IL‑8 (CXCL8) in OSCC cells; then the elevated IL‑8 bound to CXCR1 to enhance IL‑2 production and activate JAK/STAT5A pathway. These actions finally promoted OSCC development in an ectopic tumor mouse model, while knockout of IL‑8 or blocking its binding to CXCR1 compromised the impacts of MRSA EVs.
Conclusion:
Our results highlight the crucial role of antibiotic-resistant bacteria and their extracellular vesicles in tumor development and provide new insights into the relationships between microbes and tumors.
