Dataset Information

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

ABSTRACT: This study aims to investigate the role of Streptococcus mutans–derived extracellular vesicles (SmEVs) in the progression of oral squamous cell carcinoma (OSCC). We integrated transcriptomics and DIA-based quantitative proteomics to systematically analyze changes in gene expression in CAL-27 cells after SmEV treatment, as well as the protein composition of SmEVs. Our findings demonstrate that SmEVs significantly activate the Wnt/β-catenin signaling pathway, and several vesicular proteins with potential β-catenin interactions were identified. In vivo experiments further confirmed that SmEVs promote tumor growth. This project provides a proteomic dataset of SmEVs in OSCC progression, offering a new molecular resource for understanding microbe–host interactions in cancer.

ORGANISM(S): Streptococcus Mutans

SUBMITTER: Yong Fang

PROVIDER: PXD072344 | iProX | Tue Dec 23 00:00:00 GMT 2025

REPOSITORIES: iProX

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

Cao Guoding G Jiang Yichen Y Li Xinhang X Liu Ran R Liu Kaili K Balcha Fikadu F Ding Mingyang M Yuan Meng M Li Ting T Fang Yong Y

Scientific reports 20260417 1

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 ...[more]

PMID: 41991997

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Project description:Tumor: tumor microenvironment (TME) interactions are critical for tumor progression and the composition and structure of the local extracellular matrix (ECM) are key determinants of tumor metastasis. We recently reported that activation of Wnt/beta- catenin signaling in Ewing sarcoma cells induces widespread transcriptional changes that are associated with acquisition of a metastatic tumor phenotype. Significantly, ECM protein-encoding genes were found to be enriched among Wnt/beta-catenin induced transcripts, leading us to hypothesize that activation of canonical Wnt signaling might induce changes in the Ewing sarcoma secretome. To address this hypothesis, conditioned media from Ewing sarcoma cell lines cultured in the presence or absence of Wnt3a was collected for proteomic analysis. Label-free mass spectrometry was used to identify and quantify differentially secreted proteins. We then used in silico databases to identify only proteins annotated as secreted. Comparison of the secretomes of two Ewing sarcoma cell lines revealed numerous shared proteins, as well as a degree of heterogeneity, in both basal and Wnt-stimulated conditions. Gene set enrichment analysis of secreted proteins revealed that Wnt stimulation reproducibly resulted in increased secretion of proteins involved in ECM organization, ECM receptor interactions, and collagen formation. In particular, Wnt-stimulated Ewing sarcoma cells upregulated secretion of structural collagens, as well as matricellular proteins, such as the metastasis-associated protein, tenascin C (TNC). Interrogation of published databases confirmed reproducible correlations between Wnt/beta-catenin activation and TNC and COL1A1 expression in patient tumors. In summary, this first study of the Ewing sarcoma secretome reveals that Wnt/beta-catenin activated tumor cells upregulate secretion of ECM proteins. Such Wnt/beta-catenin mediated changes are likely to impact on tumor: TME interactions that contribute to metastatic progression.

Dataset Information

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

Publications

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

Similar Datasets

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