Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway
Background Recent studies reported the role of Porphyromonas gingivalis (P. g) in promoting oral squamous cell carcinoma (OSCC) progression. However, the molecular mechanism remains unclear.Materials and methods P. g-OMVs were isolated using ultracentrifugation method and characterized by transmissi...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2025-12-01
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| Series: | Journal of Oral Microbiology |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/20002297.2025.2482924 |
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| Summary: | Background Recent studies reported the role of Porphyromonas gingivalis (P. g) in promoting oral squamous cell carcinoma (OSCC) progression. However, the molecular mechanism remains unclear.Materials and methods P. g-OMVs were isolated using ultracentrifugation method and characterized by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). CCK-8, migration, invasion, Quantitative real-time Polymerase Chain Reaction (qRT-PCR) and immunocytochemistry assays were performed to evaluate the effect of P. g-OMVs on tumor cells’ proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and ferroptosis in vitro. Western blot was performed to study the phosphorylation of transcription factor nuclear factor kappa B (NF-κB). In vivo, the effect of P. g-OMVs on the growth of OSCC was evaluated using a xenograft tumor model, followed by hematoxylin and eosin and immunohistochemistry staining.Results TEM and NTA demonstrated that P. g-OMVs have a vesicular structure with a particle size of around 118 nm. Compared to the control group, P. g-OMVs significantly enhance the proliferation, migration, and invasion of tumor cells. In addition, P. g-OMVs promote the EMT of OSCC cells, which can be attenuated by ferroptosis activator erastin. Moreover, P. g-OMVs inhibit feroptosis of OSCC by activating NF-κB signaling. In vivo, P. g-OMVs significantly enhance tumor growth of OSCC. Inhibition of NF-κB could significnatly reduce the growth of OSCC, which can be further rescued using ferroptosis inhibitor Ferrostain-1.Conclusions P. g-OMVs promote OSCC progression by modulating the ferroptosis-related EMT through NF-κB signaling. |
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| ISSN: | 2000-2297 |