ArticleJournal of dental sciences2026
Cancer-associated fibroblast-derived interleukin-6 as a key driver of epithelial-mesenchymal transition and metastasis in oral squamous cell carcinoma.
Article in Journal of dental sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Matrix Stiffness Drives Aggressive Phenotype in Tongue Squamous Cell Carcinoma via Mechanotransduction-Stromal Signalling.International dental journal · 2026Article
- Effect of Indirect Co-Culture With Gingival Mesenchymal Stem Cells on Cytokine Secretion in Primary Oral Squamous Cell Carcinoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Oral squamous cell carcinoma (OSCC) is a highly metastatic cancer with a poor prognosis, partly driven by epithelial-mesenchymal transition (EMT). Although several cytokines have been implicated in OSCC progression, the specific role of cancer-associated fibroblast (CAF)-derived interleukin-6 (IL-6) in EMT and metastasis remains poorly understood. This study investigated the contribution of CAF-derived IL-6 to the promotion of EMT and metastasis in OSCC. Materials and methods: Conditioned media from gingival fibroblasts (GF) treated with OSCC-conditioned media (SCC25-GF CM) were analyzed using secretomic and functional assays. EMT marker expression, migration, and invasion were evaluated by RT-qPCR, Western blotting, immunofluorescence, and an IL-6 neutralizing antibody. Results: SCC25-GF CM significantly downregulated E-cadherin and upregulated N-cadherin, vimentin, and Snail expression, indicating EMT induction. Secretome analysis revealed elevated levels of multiple EMT- and metastasis-associated factors, including stromelysin-1, glia-derived nexin, tenascin, procathepsin L, and IL-6, in SCC25-GF CM. IL-6 neutralization reduced EMT marker expression, migration, and invasion in SCC25 cells, demonstrating that IL-6 is a key driver of CAF-mediated EMT in OSCC. Conclusion: These findings indicate that IL-6 is a central mediator of CAF-induced EMT and contributes to the metastatic potential of OSCC, highlighting IL-6 as a promising therapeutic target.
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