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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| Format: | Article |
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Taylor & Francis Group
2025-12-01
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| Series: | Journal of Oral Microbiology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/20002297.2025.2482924 |
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| author | Xinyue Liao Hang Si Yongxian Lai Xiaoyan Zhang Yun Feng Tiejun Zhou Yan Feng Li Yu |
| author_facet | Xinyue Liao Hang Si Yongxian Lai Xiaoyan Zhang Yun Feng Tiejun Zhou Yan Feng Li Yu |
| author_sort | Xinyue Liao |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-cf7f8a2160ef4918b24cbb2751295e8b |
| institution | OA Journals |
| issn | 2000-2297 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Journal of Oral Microbiology |
| spelling | doaj-art-cf7f8a2160ef4918b24cbb2751295e8b2025-08-20T02:15:20ZengTaylor & Francis GroupJournal of Oral Microbiology2000-22972025-12-0117110.1080/20002297.2025.2482924Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathwayXinyue Liao0Hang Si1Yongxian Lai2Xiaoyan Zhang3Yun Feng4Tiejun Zhou5Yan Feng6Li Yu7Department of Pediatric Dentistry, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, ChinaDepartment of Pediatric Dentistry, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, ChinaOral & Maxillofacial Reconstruction and Regeneration of Luzhou Key Laboratory, Luzhou, ChinaOral & Maxillofacial Reconstruction and Regeneration of Luzhou Key Laboratory, Luzhou, ChinaDepartment of Pediatric Dentistry, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, ChinaDepartment of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, ChinaDepartment of Pediatric Dentistry, The Affiliated Stomatology Hospital of Southwest Medical University, Luzhou, ChinaOral & Maxillofacial Reconstruction and Regeneration of Luzhou Key Laboratory, Luzhou, ChinaBackground 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.https://www.tandfonline.com/doi/10.1080/20002297.2025.2482924Porphyromonas gingivalisouter membrane vesiclesferroptosisepithelial-mesenchymal transitionoral squamous cell carcinoma |
| spellingShingle | Xinyue Liao Hang Si Yongxian Lai Xiaoyan Zhang Yun Feng Tiejun Zhou Yan Feng Li Yu Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway Journal of Oral Microbiology Porphyromonas gingivalis outer membrane vesicles ferroptosis epithelial-mesenchymal transition oral squamous cell carcinoma |
| title | Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway |
| title_full | Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway |
| title_fullStr | Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway |
| title_full_unstemmed | Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway |
| title_short | Porphyromonas gingivalis-OMVs promote the epithelial-mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the NF-κB pathway |
| title_sort | porphyromonas gingivalis omvs promote the epithelial mesenchymal transition of oral squamous cell carcinoma by inhibiting ferroptosis through the nf κb pathway |
| topic | Porphyromonas gingivalis outer membrane vesicles ferroptosis epithelial-mesenchymal transition oral squamous cell carcinoma |
| url | https://www.tandfonline.com/doi/10.1080/20002297.2025.2482924 |
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