ArticleMolecular biotechnology2024
METTL3 Mediated MALAT1 m6A Modification Promotes Proliferation and Metastasis in Osteosarcoma Cells.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 17 citations in OpenAlex.
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- Harnessing natural RNA triplex elements found in lncRNAs MALAT1 and NEAT1 for engineering of novel riboswitch platforms.Nucleic acids research · 2026Article
- MCellular oncology (Dordrecht, Netherlands) · 2026Article
- METTL3-mediated mJournal of translational medicine · 2026Article
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- RGS1 stabilized by METTL3-mediated m6A modification promotes the tumorigenicity and macrophage M2 polarization in osteosarcoma.Journal of bone oncology · 2025Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- The crosstalk of mTrends in biochemical sciences · 2025Review
- Electroacupuncture Serum Alleviates Ogd/R-Induced Astrocyte Damage by Regulating the AQP4 Via m6A Methylation of lncRNA MALAT1.Neurochemical research · 2025Article
- The METTL3/TGF-β1 signaling axis promotes osteosarcoma progression by inducing MSC differentiation into CAFs via mJournal of bone oncology · 2025Article
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- The paradoxical role of stem cells in osteosarcoma: from pathogenesis to therapeutic breakthroughs.Frontiers in oncology · 2025Review
- Long noncoding RNA MALAT1 mediates fibrous topography-driven pathologic calcification through trans-differentiation of myoblasts.Materials today. Bio · 2024Article
- METTL3 promotes the progression of osteosarcoma through the N6-methyladenosine modification of MCAM via IGF2BP1.Biology direct · 2024Article
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- Targeting lncRNA MALAT1: A Promising Approach to Overcome Metabolic Syndrome.International journal of endocrinology · 2024Review
- LncRNAs as potential prognosis/diagnosis markers and factors driving drug resistance of osteosarcoma, a review.Frontiers in endocrinology · 2024Review
- The Expression Patterns and Implications ofInternational journal of molecular sciences · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs one of the most ubiquitous types of posttranscriptional modification, N6-methyladenosine (m6A) is extensively implicated in almost all types of cancers, including osteosarcoma. Our previous research partially uncovered the role of Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) in osteosarcoma. However, the relationships between methyltransferase-like 3 (METTL3) and noncoding RNAs modified by METTL3, especially MALAT1, in osteosarcoma remain obscure.
methodsThe expression of METTL3 in osteosarcoma was evaluated by online bioinformatics analysis, immunohistochemical (IHC) staining, western blotting (WB), and reverse transcription-quantitative PCR (RT‒qPCR). Cell Counting Kit 8 (CCK-8) and Transwell assays were used to evaluate the cell proliferation and invasion abilities. The expression of MALAT1 in osteosarcoma was evaluated by online bioinformatics analysis and RT‒qPCR analysis. m6A methylated RNA immunoprecipitation-qPCR (MeRIP-qPCR) was used to detect m6A modification changes in MALAT1. An actinomycin D assay was used to study changes in the stability of MALAT1.
resultsMETTL3 was upregulated in osteosarcoma tissues and cell lines. Functionally, METTL3 promoted the proliferation and migration of osteosarcoma cells. Moreover, a clear positive correlation was found between METTL3 and MALAT1 expression, and MALAT1 was upregulated in osteosarcoma tissues and cells. Mechanistically, the presence of m6A modification sites in MALAT1 and METTL3-mediated m6A modification increased the stability of MALAT1 in osteosarcoma cells and promoted their proliferation and migration.
conclusionIn this study, it was concluded that in osteosarcoma cells, METTL3, acting as an oncogene, promoted m6A modification of MALAT1, increased the stability of MALAT, and enhanced MALAT1-mediated oncogenic function.
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