ArticleJournal of cellular and molecular medicine2020
METTL3 promotes IL-1β-induced degeneration of endplate chondrocytes by driving m6A-dependent maturation of miR-126-5p.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Involvement of the miR-128-3p/KDM3A/NLRP3 Axis in High Glucose-Induced Inflammatory Injury in Retinal Endothelial Cells.The Kaohsiung journal of medical sciences · 2026Article
- E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Circ_0070987 Promotes Pyroptosis of Ovarian Granulosa Cells in Polycystic Ovarian Syndrome Through the miR-139-5/CDH1 Axis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Regulatory roles of 13 types of RNA modifications in osteoarthritis: based on bulk and single-cell RNA analysis.3 Biotech · 2025Article
- NJournal of orthopaedic translation · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- RNA Modifications in Osteoarthritis: Epitranscriptomic Insights into Pathogenesis and Therapeutic Targets.International journal of molecular sciences · 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
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- mBiomaterials translational · 2025Review
- METTL14 is Involved in TNF-α-Induced Inflammation in Colorectal Epithelial Cells via Autophagy Modulation.Applied biochemistry and biotechnology · 2024Article
- Transcriptome-wide RNA m6A methylation profiles in an endemic osteoarthropathy, Kashin-Beck disease.Journal of cellular and molecular medicine · 2024Article
- N6-methyladenosine-driven miR-143/145-KLF4 circuit orchestrates the phenotypic switch of pulmonary artery smooth muscle cells.Cellular and molecular life sciences : CMLS · 2024Article
- N6-methyladenosine (m6A) methyltransferase WTAP-mediated miR-92b-5p accelerates osteoarthritis progression.Cell communication and signaling : CCS · 2023Article
- Diagnostic value and immune infiltration characterization of YTHDF2 as a critical m6A regulator in osteoarthritic synovitis.Journal of orthopaedic surgery and research · 2023Article
- Methyltransferase-like 3 facilitates lung cancer progression by accelerating m6A methylation-mediated primary miR-663 processing and impeding SOCS6 expression.Journal of cancer research and clinical oncology · 2022Article
- Novel insights into the interaction between N6-methyladenosine methylation and noncoding RNAs in musculoskeletal disorders.Cell proliferation · 2022Review
- Extracellular vesicles derived from human umbilical cord mesenchymal stem cells alleviate osteoarthritis of the knee in mice model by interacting with METTL3 to reduce m6A of NLRP3 in macrophage.Stem cell research & therapy · 2022Article
- METTL3 Intensifies the Progress of Oral Squamous Cell Carcinoma via Modulating the m6A Amount of PRMT5 and PD-L1.Journal of immunology research · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
METTL3 is an important regulatory molecule in the process of RNA biosynthesis. It mainly regulates mRNA translation, alternative splicing and microRNA maturation by mediating m6A-dependent methylation. Interleukin 1β (IL-1β) is an important inducer of cartilage degeneration that can induce an inflammatory cascade reaction in chondrocytes and inhibit the normal biological function of cells. However, it is unclear whether IL-1β is related to METTL3 expression or plays a regulatory role in endplate cartilage degeneration. In this study, we found that the expression level of METTL3 and methylation level of m6A in human endplate cartilage with different degrees of degeneration were significantly different, indicating that the methylation modification of m6A mediated by METTL3 was closely related to the degeneration of human endplate cartilage. Next, through a series of functional experiments, we found that miR-126-5p can play a significant role in IL-1β-induced degeneration of endplate chondrocytes. Moreover, we found that miR-126-5p can inhibit the PI3K/Akt signalling pathway by targeting PIK3R2 gene, leading to the disorder of cell vitality and functional metabolism. To further determine whether METTL3 could regulate miR-126-5p maturation, we first confirmed that METTL3 can bind the key protein underlying pri-miRNA processing, DGCR8. Additionally, when METTL3 expression was inhibited, the miR-126-5p maturation process was blocked. Therefore, we hypothesized that METTL3 can promote cleavage of pri-miR-126-5p and form mature miR-126-5p by combining with DGCR8.
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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.