ArticleBiochemistry and biophysics reports2024
The TGF-β/MMP9/RAGE axis induces sRAGE secretion by neutrophils and promotes oral carcinogenesis.
Article in Biochemistry and biophysics reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Transcriptomic Profiling of the Immune Response in Orthotopic Pancreatic Tumours Exposed to Combined Boiling Histotripsy and Oncolytic Reovirus Treatment.Pharmaceutics · 2025Article
- N2 Neutrophils and Tumor Progression in Breast Cancer: Molecular Pathways and Implications.Breast cancer (Dove Medical Press) · 2025Review
- Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025Review
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Authors and funding
8 authors.
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Abstract
In the tumor microenvironment, transforming growth factor β (TGF-β) contributes to neutrophil development toward a pro-tumor phenotype; however, the molecular mechanism by which this occurs remains unclear. Therefore, we explored the role of TGF-β in N2 neutrophil polarization and the subsequent effect on oral leukoplakia/oral squamous cell carcinoma (OL/OSCC) cells. The TGF-β-stimulated N2 culture supernatant promoted the proliferation of OL/OSCC cells. Analysis of the N2 supernatant using a cytokine array revealed significantly upregulated expression of soluble forms of receptor for advanced glycation end products (RAGE). TGF-β was found to induce the expression of RAGE and matrix metalloproteinase 9 (MMP9) in neutrophils. Additionally, MMP9 treatment could cleave RAGE and promote its secretion by neutrophils, thereby promoting cancer cell proliferation. In an established mouse model of oral cancer using 4NQO, RAGE were found to be highly expressed. Importantly, neutralizing antibodies against RAGE significantly inhibited oral cancer progression in mice. Analysis of clinical data from the TCGA database revealed that RAGE and MMP9 are highly expressed in head and neck squamous cell carcinoma (HNSCC) and that RAGE expression is significantly positively correlated with neutrophil infiltration. In conclusion, our results indicate that TGF-β promotes N2 neutrophil polarization through upregulation of soluble RAGE (sRAGE) secretion, leading to OSCC cell proliferation. Our findings also suggest that the sRAGE formed during N2 polarization may be a potential therapeutic target in OL/OSCC.
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