ArticleCell and tissue research2022
METTL3-mediated LINC00657 promotes osteogenic differentiation of mesenchymal stem cells via miR-144-3p/BMPR1B axis.
Article in Cell and tissue research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed.
- Mechanism study of METTL3 regulating Wnt/β-Catenin signalling in Pg.LPS-stimulated hSCAPs odontogenic differentiation.Molecular biology reports · 2026Article
- mMolecular medicine reports · 2026Review
- Integrative Analysis and Experimental Validation Identify Potential m6A-Related Biomarkers for Osteoporosis.Genes · 2026Article
- The progress of m6A methylation-regulated non-coding RNAs in osteogenic differentiation and osteoporosis.Non-coding RNA research · 2026Review
- METTL14 Promotes the Osteogenic Differentiation of Human Bone Marrow Stromal Cells via m6A-Dependent Stabilization of USP7 mRNA.Biochemical genetics · 2026Article
- RNA modifications: molecular orchestrators of wound healing.Burns & trauma · 2026Article
- METTL3 inhibits LINC00312 to suppress osteoporosis progression in a YTHDF2‑dependent manner.International journal of molecular medicine · 2026Article
- METTL3 inhibits osteoporosis by promoting osteoblast differentiation through m6A-mediated activation of the FZD3/RUNX1 signaling axis.European journal of medical research · 2025Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Identification and validation ofBiomolecules & biomedicine · 2025Article
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- From bone marrow mesenchymal stem cells to diseases: the crucial role of mStem cell research & therapy · 2025Review
- Regulation of Skeletogenic Pathways by m6A RNA Modification: A Comprehensive Review.Calcified tissue international · 2025Review
- METTL3-mediated m6A modification of circSTAT6 modulates miR-188-3p/Beclin1 axis to promote osteogenic differentiation of mesenchymal stem cells.Journal of orthopaedic surgery and research · 2025Article
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- Epigenetic Mechanisms in Osteoporosis: Exploring the Power of mJournal of cellular and molecular medicine · 2025Review
- mBiomaterials translational · 2025Review
- m6A methylation: a new frontier in epilepsy research and therapeutics.EXCLI journal · 2025Review
- Unraveling the Role of N6-Methylation Modification: From Bone Biology to Osteoporosis.International journal of medical sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) modification plays a crucial role in the progression of osteoporosis (OP). The study aimed to explore the effects of methyltransferase-like 3 (METTL3) in OP. The levels of METTL3, LINC00657, miR-144-3p and BMPR1B were detected using qPCR. Osteogenesis was assessed using alizarin red and alkaline phosphatase (ALP) staining assays. The protein expression of Bglap, Runx2 and Col1a1 was measured by western blot. The targets of LINC00657 and miR-144-3p were screened by bioinformatic analysis. The interaction between miR-144-3p and LINC00657 or BMPR1B was analyzed by dual-luciferase reporter assay and RNA pull-down assay. The results showed that METTL3 was downregulated in OP. METTL3 mediated m6A methylation of LINC00657 to promote the development of osteogenesis. Further study indicated that LINC00657 functioned as a ceRNA to upregulate BMPR1B via sponging miR-144-3p. Additionally, BMPR1B knockdown alleviated the effects of METTL3 on osteogenesis of bone marrow mesenchymal stem cells (BMSCs). Taken together, METTL3 facilitated osteogenic differentiation of BMSCs via the LINC00657/miR-144-3p/BMPR1B axis. Our findings may provide a novel insight of m6A methylation in the development of OP.
Indexed as
Identifiers
35192037What Socratic 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 Socratic graph.