Article3 Biotech2026
Arecoline promotes oral submucous fibrosis by enhancing epithelial cell cuproptosis through PUS1-mediated pseudouridylation.
Article in 3 Biotech, 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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4 authors.
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Abstract
Oral submucous fibrosis (OSF) is a chronic, potentially malignant disorder strongly associated with areca nut chewing. Cuproptosis, a newly identified form of cell death, may play a role in OSF progression, but the mechanisms remain unclear. This study aimed to explore the involvement of cuproptosis in OSF. Here, we observed a significant increase in cuproptosis markers (FDX1 and LIAS) in OSF lesion tissues compared to normal oral mucosa. In vitro, arecoline induced cuproptosis predominantly in epithelial cells, characterized by increased FDX1 and LIAS expression, disrupted lipoylation of DLAT, and elevated intracellular Cu²⁺ accumulation. An epigenetic modification PCR array revealed that arecoline most markedly upregulated PUS1, a pseudouridine (Ψ) modification synthase. Functional knockdown of PUS1 alleviated arecoline-induced cuproptosis, as evidenced by reduced Cu²⁺ levels and restored lipoic acid expression. Dot blot and PA-ψ-seq further demonstrated that arecoline-induced PUS1 upregulation altered the global tRNA pseudouridylation landscape, with enrichment of Ψ peaks in Wnt- and copper transport-related transcripts. PUS1 knockdown markedly attenuated arecoline-induced β-catenin nuclear localization and the upregulation of MYC, FZD6, CTNNB1, NFAT5, SLC25A39, and VDAC2. In conclusion, we reveal a previously unrecognized mechanism whereby arecoline promotes OSF via PUS1-dependent pseudouridylation remodeling and epithelial cuproptosis, offering novel therapeutic targets for OSF intervention. Supplementary Information: The online version contains supplementary material available at 10.1007/s13205-026-04931-8.
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