ArticleGenes & genomics2022
Methyltransferase-like 3 (METTL3) mediated N6-methyladenosine (m6A) modifications facilitate mir-25-3p maturation to promote gastrointestinal stromal tumors (GISTs) progression.
Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Non-Coding RNAs in Gastrointestinal Stromal Tumors: Regulatory Networks, Drug Resistance, and Clinical Implications.International journal of molecular sciences · 2026Review
- miR-25-3p Modulates Tumor Aggressiveness and Ferroptosis Escape in T24 Bladder Cancer Cells In Vitro.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Recent advances in noncoding RNA modifications of gastrointestinal cancer.Cancer science · 2025Review
- METTL3 accelerates staphylococcal protein A (SpA)-induced osteomyelitis progression by regulating m6A methylation-modified miR-320a.Journal of orthopaedic surgery and research · 2024Article
- KIT mutations and expression: current knowledge and new insights for overcoming IM resistance in GIST.Cell communication and signaling : CCS · 2024Review
- N6-Methyladenosine in Cell-Fate Determination of BMSCs: From Mechanism to Applications.Research (Washington, D.C.) · 2024Article
- The METTL3/miR-196a Axis Predicts Poor Prognosis in Non-small Cell Lung Cancer.Journal of Cancer · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMethyltransferase-like 3 (METTL3) is an RNA N6-methyladenosine (m6A) methyltransferase, which plays a critical role in micorRNA (miRNAs) processing and maturation, but it is still unclear whether METTL3 regulated miRNAs participates in the regulation of cancer aggressiveness in gastrointestinal stromal tumors (GISTs).
objectivesThis study was designed to investigate this issue, and uncover the potential underlying mechanisms.
methodsthe expression of METTL3 in GISTs tissues and cell lines were determined by RT-qPCR and Western blot. Cell proliferation and migration were assessed by colony formation, CCK-8 and Transwell. The mRNA expression of all proteins was detected by RT-qPCR, and tumor xenograft study was applied to confirm the effect of METTL3 on GISTs development in vivo.
resultsIn our study, we showed that METTL3 was significantly upregulated in GISTs tissues and cell lines. Functional experiments demonstrated that overexpression of METTL3 promoted GISTs cell malignant biological behavior and tumor growth in vitro and in vivo, and conversely, silencing of METTL3 had opposite effects and suppressed GISTs progression. Further mechanistical experiments verified that METTL3 promoted the maturation of miR-25-3p in an m6A-dependent manner. Similar to METTL3, miR-25-3p was also validated as an oncogene to promote cancer development in GISTs. Finally, our rescuing experiments hinted that silencing of miR-25-3p abrogated the tumor-initiating effects of METTL3 overexpression on GISTs.
conclusionCollectively, those results indicated that METTL3 played an oncogenic role in GISTs through positively modulating the miR-25-3p in an m6A-dependent manner, and we firstly discussed how the METTL3/m6A/miR-25-3p axis affected GISTs development.
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