ArticleMolecular biology reports2025
The N-terminal domain of precursor IL-1α enhances IL-6 expression via an intracrine mechanism in oral squamous cell carcinoma.
Article in Molecular biology reports, 2025. 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
introductionInterleukin-1α (IL-1α) is a pleiotropic cytokine that functions both extracellularly and intracellularly; however, the mechanisms by which precursor IL-1α (pIL-1α) contributes to cytokine regulation in oral squamous cell carcinoma (OSCC) remain unclear.
methodsTo elucidate the intracellular role of pIL-1α, IL-1α knockout (KO) cells (designated α7) were established from HSC-3 OSCC cells. Reconstitution experiments were performed using constructs expressing pIL-1α, mature IL-1α (mIL-1α), or an N-terminal propiece (ppIL-1α). The Δ nuclear localization sequence (NLS) mutant was used to evaluate the functional relevance of nuclear localization.
resultsα7 cells exhibited significantly diminished secretion of IL-6, IL-8, and IL-1β relative to the parental cells. Reexpression of full-length pIL-1α selectively restored IL-6 expression, whereas neither mIL-1α nor ppIL-1α alone had this effect. The ΔNLS mutant was retained in the cytoplasm and failed to upregulate IL-6, indicating its necessity for its nuclear localization. Exogenous recombinant IL-1α did not induce IL-6 expression in HSC-3 cells, suggesting a receptor-independent regulation.
conclusionThese findings delineate a non-canonical intracrine mechanism by which pIL-1α, via its N-terminal NLS-containing domain, translocates to the nucleus and regulates IL-6 gene expression independent of IL-1 receptor signaling. This study provides new insights into the intracellular functions of IL-1α in inflammatory and tumorigenic processes and suggests potential therapeutic avenues targeting its nuclear trafficking.
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