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Objective <p>To investigate the mechanism of action of <i>Porphyromonas gingivalis</i> (<i>P. gingivalis</i>) and <i>Fusobacterium nucleatum</i> (<i>F. nucleatum</i>) individually and synergistically on Cal-27 cells through transcriptome analyses to evaluate the mechanism evidence of periodontal pathogen involvement in oral squamous cell carcinoma.</p> Methods <p>Cal-27 cells were treated with <i>P. gingivalis</i> and <i>F. nucleatum</i> individually or in combination. Cell proliferation was assessed via CCK-8 assay and EdU staining, while migration was evaluated using scratch assays. Transcriptomic sequencing analyzed molecular mechanisms underlying single and co-infections.</p> Results <p>Synergistic treatment with <i>P. gingivalis</i> and <i>F. nucleatum</i> significantly enhanced Cal-27 cell proliferation and migration compared to either pathogen alone. Transcriptomics revealed that co-infection accelerated tumor cell cycle progression and amplified pro-inflammatory pathways, indicating stronger pro-tumorigenic effects.</p> Conclusion <p>This study clarifies the cooperative tumor-promoting role of multiple bacterial species, providing potential therapeutic targets for oral squamous cell carcinoma in bacterial infection contexts and highlighting the importance of controlling oral microbiota.</p>

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Porphyromonas gingivalis and Fusobacterium nucleatum synergistically strengthen the effect of promoting oral squamous cell carcinoma progression

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月29日

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  • Xiao Song,
  • Jingfei Wang,
  • Zhen Gu,
  • Xinyi Qiu,
  • Meng Yuan,
  • Huiji Ke,
  • Runzhi Deng

摘要

Objective

To investigate the mechanism of action of Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) individually and synergistically on Cal-27 cells through transcriptome analyses to evaluate the mechanism evidence of periodontal pathogen involvement in oral squamous cell carcinoma.

Methods

Cal-27 cells were treated with P. gingivalis and F. nucleatum individually or in combination. Cell proliferation was assessed via CCK-8 assay and EdU staining, while migration was evaluated using scratch assays. Transcriptomic sequencing analyzed molecular mechanisms underlying single and co-infections.

Results

Synergistic treatment with P. gingivalis and F. nucleatum significantly enhanced Cal-27 cell proliferation and migration compared to either pathogen alone. Transcriptomics revealed that co-infection accelerated tumor cell cycle progression and amplified pro-inflammatory pathways, indicating stronger pro-tumorigenic effects.

Conclusion

This study clarifies the cooperative tumor-promoting role of multiple bacterial species, providing potential therapeutic targets for oral squamous cell carcinoma in bacterial infection contexts and highlighting the importance of controlling oral microbiota.