ArticleJournal of dental sciences2025
Silencing miR-1291-LEFTY2 axis diminishes the myofibroblast activities and reactive oxygen species generation of fibrotic buccal mucosal fibroblasts.
Article in Journal of dental sciences, 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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6 authors.
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Abstract
Background/purpose: Oral submucous fibrosis (OSF) is a potentially malignant disorder characterized by chronic inflammation and excessive collagen deposition, leading to fibrosis in the oral mucosa. This study aimed to explore the contribution of the miR-1291/LEFTY2 axis in the development of OSF progression. Materials and methods: Expression of miR-1291 was evaluated in OSF tissues and primary myofibroblasts using RNA sequencing and qRT-PCR. The functional role of miR-1291 and LEFTY2 were investigated using miR-1291 inhibitor and lentiviral-mediated overexpression of LEFTY2, respectively. A luciferase reporter assay was conducted to examine the direct interaction between miR-1291 and LEFTY2. Myofibroblast activities were assessed by collagen gel contraction, wound healing, and transwell migration assays. Reactive oxygen species (ROS) production was measured by flow cytometry. Results: MiR-1291 was markedly upregulated in OSF tissues and myofibroblasts, and it was positively correlated with a couple of fibrosis markers, including α-SMA and TGF-β1. Inhibition of miR-1291 suppressed myofibroblast activities and ROS generation. Luciferase reporter assays confirmed that miR-1291 is directly bound to the three prime untranslated region (3'UTR) of LEFTY2, a negative regulator of TGF-β signaling. Overexpression of LEFTY2 attenuated phosphorylation of Smad, myofibroblast activities, and ROS production. Conclusion: Our findings demonstrated that miR-1291 may promote fibrosis in OSF by suppressing LEFTY2 expression to increase myofibroblast activation via regulation of ROS accumulation and TGF-β/Smad signaling.
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