ArticleAging2021
METTL14 benefits the mesenchymal stem cells in patients with steroid-associated osteonecrosis of the femoral head by regulating the m6A level of PTPN6.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- Recent advances in osteonecrosis of the femoral head: a focus on mesenchymal stem cells and adipocytes.Journal of translational medicine · 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
- Epigenetic modification mediated by PHF20/METTL14/HOXA13 signaling axis modulates osteogenic differentiation of mesenchymal stem cells.Functional & integrative genomics · 2025Article
- Epigenetic Mechanisms in Osteoporosis: Exploring the Power of mJournal of cellular and molecular medicine · 2025Review
- Targeting protein tyrosine phosphatase non-receptor type 6 (PTPN6) as a therapeutic strategy in acute myeloid leukemia.Cell biology and toxicology · 2024Article
- Wilms tumor 1-associated protein mediated m6A modification promotes osteogenic differentiation of stem cells from human exfoliated deciduous teeth.Journal of dental sciences · 2024Article
- METTL7A-mediated m6A modification of corin reverses bisphosphonates-impaired osteogenic differentiation of orofacial BMSCs.International journal of oral science · 2024Article
- YTHDF2-Mediated m6A methylation inhibition by miR27a as a protective mechanism against hormonal osteonecrosis in BMSCs.BMC musculoskeletal disorders · 2024Article
- m6A methylation modification and immune infiltration analysis in osteonecrosis of the femoral head.Journal of orthopaedic surgery and research · 2024Article
- N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications.Research (Washington, D.C.) · 2024Article
- Compression Promotes the Osteogenic Differentiation of Human Periodontal Ligament Stem Cells by Regulating METTL14-mediated IGF1.Current stem cell research & therapy · 2024Article
- Epitranscriptomic modifications in mesenchymal stem cell differentiation: advances, mechanistic insights, and beyond.Cell death and differentiation · 2024Review
- The essential roles of mGenes & diseases · 2024Review
- mActa biochimica et biophysica Sinica · 2023Review
- The m6A methyltransferase METTL16 negatively regulates MCP1 expression in mesenchymal stem cells during monocyte recruitment.JCI insight · 2023Article
- Deciphering the map of METTL14-mediated lncRNA m6A modification at the transcriptome-wide level in breast cancer.Journal of clinical laboratory analysis · 2022Article
- Bioinformatics gene analysis of potential biomarkers and therapeutic targets of osteoarthritis associated myelodysplastic syndrome.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imbalanced osteogenic/adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is considered the core pathological characteristic of steroid-associated osteonecrosis of the femoral head (SONFH). N6-Methyladenosine (m6A) is the most common type of RNA modification in eukaryotic cells and participates in various physiological and pathological processes. However, the relationship between m6A modification and SONFH has not been reported. In the present study, we aimed to explore the roles of m6A modifications and methyltransferase METTL14 in SONFH. Our results showed that the m6A levels were down-regulated in femoral head tissues and BMSCs from SONFH patients, and this effect was attributed to the reduction of METTL14. Furthermore, METTL14 overexpression in BMSCs from SONFH patients enhanced cell proliferation and osteogenic differentiation. We further identified PTPN6 as the downstream target of METTL14 by mRNA sequencing. Mechanistically, METTL14 regulated PTPN6 expression by increasing PTPN6 mRNA stability in an m6A-dependent manner. Moreover, PTPN6 knockdown abrogated the beneficial effects of METTL14 overexpression on BMSCs. Additionally, we found that METTL14 activated the Wnt signaling pathway, and this effect was caused by the interaction of PTPN6 and GSK-3β. In conclusion, we elucidated the functional roles of METTL14 and m6A methylation in SONFH BMSCs and identified a novel RNA regulatory mechanism, providing a potential therapeutic target for SONFH.
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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.