ArticleJournal of dental sciences2026
Isoliquiritigenin represses the pro-fibrotic TGF-β/smad2 signaling and nuclear enriched abundant transcript 1 (NEAT1) in oral submucous fibrosis.
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: Isoliquiritigenin (ISL) has shown anti-fibrotic potential in several organ systems, but its effects on oral submucous fibrosis (OSF) remain unclear. This study investigated whether ISL attenuates myofibroblast activities in buccal mucosal fibroblasts (BMFs) from OSF patients by modulating TGF-β/Smad2 signaling and the long non-coding RNA NEAT1. Materials and methods: Primary normal BMFs and fibrotic BMFs (fBMFs) were isolated from human buccal mucosa, and cell viability, collagen gel contraction, migration, and wound closure were examined after ISL treatment with or without arecoline. TGF-β1 secretion was quantified, while protein expression of phosphorylated Smad2, COL1A1, and α-SMA was analyzed, and NEAT1 expression was assessed with gain-of-function experiments. Results: ISL showed selective cytotoxicity toward fBMFs compared with normal BMFs. ISL (5 and 10 μM) significantly reduced collagen gel contraction and migration capacity of fBMFs, and reversed arecoline-induced increases in contractility and migration. ISL also decreased TGF-β1 secretion and suppressed phosphorylated Smad2, COL1A1, and α-SMA expression. Furthermore, ISL downregulated NEAT1 in fBMFs, and NEAT1 overexpression enhanced collagen gel contraction, whereas ISL partially but significantly abrogated this pro-contractile effect, suggesting that NEAT1 mediates, at least in part, ISL's anti-fibrotic actions. Conclusion: In conclusion, ISL selectively targets OSF-derived fibroblasts and attenuates myofibroblast-like phenotypes by disrupting TGF-β1/Smad2 signaling and NEAT1-driven fibrogenic activity. These findings highlight ISL as a promising candidate for adjunctive therapy in OSF.
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