ArticleJournal of dental sciences2025
MicroRNA let-7a mitigates the progression of oral submucous fibrosis by targeting high-mobility group AT-hook 2.
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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Oral submucous fibrosis (OSF) is an irreversible fibrotic disorder of the oral cavity with a high potential for malignant transformation. MicroRNA lethal-7a (let-7a) has been recognized as a key antifibrotic regulator, but its specific role in OSF remains unknown. Therefore, this study aimed to elucidate the functional significance and the molecular mechanism of let-7a in OSF progression. Materials and methods: The expression of let-7a was quantified by real-time quantitative polymerase chain reaction in fibrotic buccal mucosal fibroblasts (fBMFs) isolated from OSF lesions and patient-matched non-fibrotic BMFs (BMFs). Myofibroblastic characteristics were evaluated using collagen-gel contraction, Transwell migration, and wound-healing assays. Restoration and inhibition of let-7a expression were achieved by transfecting let-7a mimics or inhibitors, respectively. Direct binding of let-7a to high-mobility group AT-hook 2 (HMGA2) mRNA was verified using luciferase reporter assay. Results: Let-7a expression was significantly down-regulated in fBMFs isolated from OSF lesions compared with patient-matched non-fibrotic BMFs. Moreover, let-7a expression declined in a dose-dependent manner during arecoline-induced myofibroblastic transdifferentiation of BMFs. Myofibroblastic characteristics, including cell contractility, cell migration, and wound-healing capacity were significantly decreased in fBMFs after transfection of let-7a mimics. Mechanistically, let-7a directly targeted the HMGA2 mRNA, leading to post-transcriptional repression of HMGA2. Importantly, silencing of HMGA2 was sufficient to diminish cell contractility and myofibroblasts marker expression in fBMFs. Conclusion: The present study demonstrates that let-7a suppresses oral myofibroblast activation by directly targeting HMGA2. This finding first establishes the let-7a/HMGA2 axis as a promising therapeutic target for mitigating the progression of OSF.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.