ArticleBioengineered2022
Methylation recognition protein YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) regulates the proliferation, migration and invasion of osteosarcoma by regulating m6A level of CCR4-NOT transcription complex subunit 7 (CNOT7).
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- Bibliometric analysis of RNA-binding proteins in osteosarcoma: unraveling research trends and hotspots.Frontiers in immunology · 2025Pooled it
- Prognostic and clinicopathological value of m6A regulators in human cancers: a meta-analysis.Aging · 2022Pooled it
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- CNOT9 affects hepatocellular carcinoma proliferation and cell cycle through the PTEN/AKT/p53 signaling pathway.Human cell · 2026Article
- The METTL3-IGF2BP3 axis drives osteosarcoma progression by enhancing ID1 mRNA stability.BMC musculoskeletal disorders · 2026Article
- CNOT7 facilitates radiation resistance in colorectal cancer through TRIM21/XRCC6-mediated non-homologous end joining repair.Cell death & disease · 2025Article
- RNA mCell investigation · 2025Article
- Methyltransferase-Like 3-Mediated NJournal of cellular and molecular medicine · 2025Review
- Research progress on N6-methyladenosine RNA modification in osteosarcoma: functions, mechanisms, and potential clinical applications.Medical oncology (Northwood, London, England) · 2025Review
- Review of the role and potential clinical value of m6A methylation modifications in the biological process of osteosarcoma.Frontiers in genetics · 2025Review
- mBiomaterials translational · 2025Review
- Epigenetic modifications in follicular cell-derived thyroid cancer: new dimensions in pathogenesis and treatment.Frontiers in oncology · 2025Review
- Influence of RNA Methylation on Cancerous Cells: A Prospective Approach for Alteration of In Vivo Cellular Composition.Advances in experimental medicine and biology · 2025Review
- METTL3 Mediated MALAT1 m6A Modification Promotes Proliferation and Metastasis in Osteosarcoma Cells.Molecular biotechnology · 2024Article
- Ramifications of m6A Modification on ncRNAs in Cancer.Current genomics · 2024Review
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
- Novel insights into the regulatory role of N6-methyladenosine methylation modified autophagy in sepsis.Aging · 2023Article
- N6-methyladenosine (m6A) modification in osteosarcoma: expression, function and interaction with noncoding RNAs - an updated review.Epigenetics · 2023Review
- Novel insights into the METTL3-METTL14 complex in musculoskeletal diseases.Cell death discovery · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is one of the most significant modifications in human mRNAs. Emerging evidence indicates that m6A participates in the initiation and development of malignant tumors. Nevertheless, the biological roles and mechanism of m6A in osteosarcoma (OS) remain unclear. The purpose of this study was to investigate the role and mechanism of the methylation recognition protein-YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) in OS. The YTHDF1 expression in OS was detected by qRT-PCR and Western blot assay. M6A quantification was utilized to measure the methylation level of OS. Cell counting kit-8 (CCK8), 5-Ethynyl-2'-deoxyuridine (EdU) assay and transwell experiments were conducted to confirm the biological effects of YTHDF1 on OS cells. The bioinformatics websites and in vitro assays were conducted to analyze the downstream targets of YTHDF1 was upregulated in OS tissues at mRNA and protein level. The results showed that the expression level of YTHDF1 might be closely associated with the poor prognosis for OS patients. Inhibition of YTHDF1 could suppress the proliferation, migration and invasion of the OS cells. Moreover, we found that CCR4-NOT transcription complex subunit 7 (CNOT7) might be the potential target of YTHDF1, which was upregulated in OS tissues. YTHDF1 could recognize the m6A sites of CONT7 and promote its expression in an m6A manner. Moreover, methyltransferase-like 3 (METTL3) could promote the m6A level of CONT7. YTHDF1 was upregulated in OS and could promote cell proliferation, migration and invasion. The METTL3-CONT7-YTHDF1 regulatory axis might be the potential target for the prognosis and therapy of OS.
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