ArticleMolecular and cellular biochemistry2020
The m6A methyltransferase METTL3 cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-κB signaling.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 96 citations in OpenAlex.
- Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management.Journal of musculoskeletal & neuronal interactions · 2026Article
- METTL3-mCellular & molecular biology letters · 2026Article
- RNA modifications: molecular orchestrators of wound healing.Burns & trauma · 2026Article
- Molecular mechanisms and translational prospects in osteoporosis.Frontiers in endocrinology · 2026Review
- ALKBH5-Mediated mMolecular biotechnology · 2025Article
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- FTOZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- METTL3 regulated by histone lactylation promotes ossification of the ligamentum flavum by enhancing the m6A methylation of BMP2.Molecular medicine (Cambridge, Mass.) · 2025Article
- Global analysis by LC-MS/MS ofRNA (New York, N.Y.) · 2025Article
- m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025Review
- ALKBH5 in development: decoding the multifaceted roles of mFrontiers in molecular biosciences · 2025Review
- mBiomaterials translational · 2025Review
- ALKBH5 Regulates Osteogenic Differentiation via the lncRNA/mRNA Complex.Journal of dental research · 2024Article
- Differentiation and Growth-Arrest-Related lncRNA (International journal of molecular sciences · 2024Article
- Complicated role of ALKBH5 in gastrointestinal cancer: an updated review.Cancer cell international · 2024Review
- Article
- N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications.Research (Washington, D.C.) · 2024Article
- The Effect Mechanism of N6-adenosine Methylation (m6A) in Melatonin Regulated LPS-induced Colon Inflammation.International journal of biological sciences · 2024Article
- Epitranscriptomic modifications in mesenchymal stem cell differentiation: advances, mechanistic insights, and beyond.Cell death and differentiation · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
As a m6A methylation modifier, METTL3 is functionally involved in various biological processes. Nevertheless, the role of METTL3 in osteogenesis is not determined up to date. In the current study, METTL3 is identified as a crucial regulator in the progression of osteogenic differentiation. Loss of METTL3 significantly augments calcium deposition and enhances alkaline phosphatase activity of mesenchymal stem cells, uncovering an inhibitory role of METTL3 in osteogenesis. More importantly, the underlying molecular basis by which METTL3 regulates osteogenesis is illustrated. We find that METTL3 positively regulates expression of MYD88, a critical upstream regulator of NF-κB signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-κB which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. Moreover, the METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5. In summary, this study highlights the functional importance of METTL3 in osteogenic differentiation and METTL3 may serve as a promising molecular target in regenerative medicine, as well as in the field of bone tissue engineering.
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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.