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<p>Oral squamous cell carcinoma (OSCC) is an aggressive malignancy in which microbial dysbiosis is increasingly recognized as a contributing factor, yet the pathogenic potential of bacterial extracellular vesicles (EVs) remains poorly defined. To determine whether Streptococcus mutans–derived EVs (SmEVs) influence OSCC progression, we isolated and characterized SmEVs from ATCC 35,668 and examined their effects in CAL-27 cells and a nude-mouse xenograft model. SmEVs were readily internalized by OSCC cells, enhancing their proliferative, migratory, and invasive capacities in vitro. Transcriptomic analysis revealed that SmEV exposure reshaped the CAL-27 gene expression landscape, prominently enriching the Wnt/β-catenin signaling pathway, accompanied by increased activation of β-catenin, TCF7, and FOSL1/Fra-1 in both cultured cells and xenograft tumors. Functional loss-of-experiments further demonstrated that β-catenin is critically required for these effects, as its silencing abrogated SmEV-induced proliferation, migration, and activation of the TCF7/Fra-1 axis. DIA proteomics identified a broad array of SmEV proteins, and in silico docking highlighted several abundant, cancer-associated candidates with strong predicted interactions with β-catenin. In <i>vivo</i>, co-administration of SmEVs accelerated tumor growth and reinforced activation of the β-catenin axis. Collectively, these findings provide the first evidence that S. mutans–derived EVs promote OSCC progression through β-catenin–driven transcriptional programs and identify specific vesicular proteins as candidate mediators, offering new insights into microbe-derived factors as potential diagnostic or therapeutic targets in OSCC.</p>

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Bacterial extracellular vesicles from Streptococcus mutans drive OSCC progression through β-catenin signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月17日

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  • Guoding Cao,
  • Yichen Jiang,
  • Xinhang Li,
  • Ran Liu,
  • Kaili Liu,
  • Fikadu Balcha,
  • Mingyang Ding,
  • Meng Yuan,
  • Ting Li,
  • Yong Fang

摘要

Oral squamous cell carcinoma (OSCC) is an aggressive malignancy in which microbial dysbiosis is increasingly recognized as a contributing factor, yet the pathogenic potential of bacterial extracellular vesicles (EVs) remains poorly defined. To determine whether Streptococcus mutans–derived EVs (SmEVs) influence OSCC progression, we isolated and characterized SmEVs from ATCC 35,668 and examined their effects in CAL-27 cells and a nude-mouse xenograft model. SmEVs were readily internalized by OSCC cells, enhancing their proliferative, migratory, and invasive capacities in vitro. Transcriptomic analysis revealed that SmEV exposure reshaped the CAL-27 gene expression landscape, prominently enriching the Wnt/β-catenin signaling pathway, accompanied by increased activation of β-catenin, TCF7, and FOSL1/Fra-1 in both cultured cells and xenograft tumors. Functional loss-of-experiments further demonstrated that β-catenin is critically required for these effects, as its silencing abrogated SmEV-induced proliferation, migration, and activation of the TCF7/Fra-1 axis. DIA proteomics identified a broad array of SmEV proteins, and in silico docking highlighted several abundant, cancer-associated candidates with strong predicted interactions with β-catenin. In vivo, co-administration of SmEVs accelerated tumor growth and reinforced activation of the β-catenin axis. Collectively, these findings provide the first evidence that S. mutans–derived EVs promote OSCC progression through β-catenin–driven transcriptional programs and identify specific vesicular proteins as candidate mediators, offering new insights into microbe-derived factors as potential diagnostic or therapeutic targets in OSCC.