ArticleJournal of dental sciences2025
GAS5 decreased the arecoline-induced myofibroblasts activity in buccal mucosal fibroblasts via acting as a competing endogenous RNA for miR-21.
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. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Oral submucous fibrosis (OSF) is recognized as a premalignant condition that increases the risk of oral cancer. Myofibroblasts are the primary cellular mediators of the pathological fibrosis characteristic of OSF. Consequently, understanding the molecular mechanisms that drive myofibroblast activation is crucial for the development of effective therapeutic interventions for this condition. Growth arrest-specific 5 (GAS5), a long non-coding RNA, represents a potential regulatory factor in OSF pathogenesis, although its specific role remains largely undefined. Materials and methods: To validate the direct interaction between GAS5 and its target miR-21, a luciferase reporter assay was performed. qRT-PCR was employed to evaluate the expression levels of GAS5 in OSF tissues. Collagen gel contraction and transwell migration assays were utilized to assess myofibroblast functional activities. Results: Our result validated overexpression of GAS5 inhibits TGF-β-induced myofibroblast activation, as evidenced by reduced collagen gel contraction, cell migration, and suppression of the TGF-β/Smad2 signaling pathway. GAS5 also attenuates arecoline-induced myofibroblast activation. Mechanistically, GAS5 directly interacts with and sponges miR-21, thereby modulating myofibroblast function. Conclusion: Our findings suggest that GAS5 plays a crucial role in inhibiting myofibroblast activation in OSF by targeting the TGF-β/Smad2 signaling pathway and regulating the miR-21. GAS5 may represent a novel therapeutic target for the prevention and treatment 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.