ArticleJournal of orthopaedic surgery and research2025
METTL3-mediated m6A modification of circSTAT6 modulates miR-188-3p/Beclin1 axis to promote osteogenic differentiation of mesenchymal stem cells.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- METTL3-mediated m6A methylation to promote mandibular condyle fracture repair via TGF-β/Smad signaling pathway.Scientific reports · 2026Article
- The progress of m6A methylation-regulated non-coding RNAs in osteogenic differentiation and osteoporosis.Non-coding RNA research · 2026Review
- Effects of the Total Flavonoids fromCurrent molecular medicine · 2026Article
- Understanding the molecular basis of mesenchymal stem cell stemness: implications for clinical applications.Cell death & disease · 2025Review
- Novel insights into the N 6-methyladenosine modification on circRNA in cancer.Frontiers in oncology · 2025Review
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Authors and funding
4 authors.
Funding
Abstract
backgroundThe role of N6-methyladenosine (m6A)-modified circRNAs in disease progression is of great significance. However, the specific impact of m6A modification of circSTAT6 on osteoporosis (OP) is still uncertain.
methodsThe qRT-PCR was employed to assess the levels of METTL3, circSTAT6, miR-188-3p, and Beclin1. To investigate the interaction between miR-188-3p and circSTAT6 or Beclin, a dual-luciferase reporter assay was performed. To evaluate osteogenic differentiation in bone marrow mesenchymal stem cell (BMSC), western blot analysis was conducted to evaluate the protein expression of osteogenic markers, including ALP, OPN, and Runx2. In addition, alizarin red and alkaline phosphatase (ALP) staining assays were employed to assess osteogenesis.
resultsThe findings revealed that the downregulation of circSTAT6 was observed in OP. On the other hand, the overexpression of circSTAT6 was found to enhance the osteogenic differentiation of BMSC. In addition, the involvement of METTL3 in mediating m6A methylation of circSTAT6 was identified, which ultimately promoted osteogenesis. Furthermore, circSTAT6 functioned as an miR-188-3p sponge to regulate the expression of Beclin1. Further study revealed that the osteogenic-enhancing effect caused by circSTAT6 overexpression was counteracted by introducing a miR-188-3p mimic. Similarly, the osteogenic-promoting impact of the miR-188-3p inhibitor was reversed by suppressing Beclin1 expression.
conclusionsThe present study revealed, for the first time, that METTL3-mediated m6A modification of circSTAT6 regulated the miR-188-3p/Beclin1 axis to promote the osteogenic differentiation of BMSC. These findings offer a potential therapeutic target for the treatment of OP.
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