ArticleJournal of dental sciences2026
Tumor microenvironment-derived IL-32 promotes aggressive phenotypes and stem cell traits in head and neck 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. Not yet cited in PubMed.
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Abstract
Background/purpose: Head and neck squamous cell carcinoma (HNSCC) is an aggressive malignancy distinguished by marked invasiveness, a high metastatic propensity, and poor prognosis. Cancer-associated fibroblasts (CAFs) within the tumour microenvironment secrete numerous mediators that accelerate tumour progression; however, the precise contribution of CAF-derived interleukin-32 (IL-32) remains unclear. This study examined the influence of CAF-derived IL-32 on invasion, epithelial-mesenchymal transition (EMT), and cancer-stem-cell (CSC) traits in HNSCC. Materials and methods: Primary CAFs and normal fibroblasts (NFs) were isolated from HNSCC specimens. IL-32 expression was quantified by microarray analysis, quantitative PCR, Western blotting, and enzyme-linked immunosorbent assay. Migration and invasion of FaDu and SCC25 cells were assessed with Transwell assays after exposure to CAF-conditioned medium or recombinant IL-32. EMT markers were evaluated by Western blotting, whereas sphere-formation assays and flow cytometry for CD133 Results: IL-32 was significantly up-regulated in CAFs compared with NFs. Both CAF-conditioned medium and recombinant IL-32 markedly increased the migratory and invasive capacities of HNSCC cells. These treatments reduced E-cadherin and increased Vimentin, Snail, and Twist expression, while enhancing sphere formation and expanding CD24 Conclusion: CAFs promote HNSCC progression through IL-32-mediated enhancement of invasion, EMT induction, and CSC properties. Targeting IL-32 signalling may represent a promising therapeutic approach to improve outcomes in HNSCC.
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