ArticleMolecular cell2025
A methyltransferase-independent role for METTL1 in tRNA aminoacylation and oncogenic transformation.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Adenosine 5'-Carboxamide-Based Inhibitors of METTL1.ACS medicinal chemistry letters · 2026Article
- METTL1/WDR4 Complex: A Novel Epitranscriptomic Target at the Crossroads of RNA Methylation and Drug Discovery.Journal of medicinal chemistry · 2026Review
- Transfer RNA expression, modification, and derived small RNAs in cancer biology and clinical potential.Frontiers in immunology · 2026Review
- Beyond RNA modification: a novel role for tRNA modifying enzyme in oxidative stress response and metabolism.Nucleic acids research · 2025Article
- Compensatory tRNA Modification by DUS3L Confers Resistance to METTL1 Loss in Oesophageal Cancer.bioRxiv : the preprint server for biology · 2025Article
- Rethinking RNA Modifications: Therapeutic Strategies for Targeting Dysregulated RNA.Journal of molecular biology · 2025Review
- METTL1 in human cancers: recognition of their functions, mechanisms and therapeutic value.Oncology reviews · 2025Review
- METTL1-driven nucleotide metabolism reprograms the immune microenvironment in hepatocellular carcinoma: a multi-omics approach for prognostic biomarker discovery.Frontiers in immunology · 2025Article
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Authors and funding
21 authors.
Funding
Abstract
Amplification of chromosomal material derived from 12q13-15 is common in human cancer and believed to result in overexpression of multiple collaborating oncogenes. To define the oncogenes involved, we overexpressed genes recurrently amplified in human liposarcoma using a zebrafish model of the disease. We found several genes whose overexpression collaborated with AKT in sarcomagenesis, including the tRNA methyltransferase METTL1. This was surprising, because AKT phosphorylates METTL1 to inactivate its enzymatic activity. Indeed, phosphomimetic S27D or catalytically dead alleles phenocopied the oncogenic activity of wild-type METTL1. We found that METTL1 binds the multi-tRNA synthetase complex, which contains many of the cellular aminoacyl-tRNA synthetases and promotes tRNA aminoacylation, polysome formation, and protein synthesis independent of its methyltransferase activity. METTL1-amplified liposarcomas were hypersensitive to actinomycin D, a clinical inhibitor of ribosome biogenesis. We propose that METTL1 overexpression promotes sarcomagenesis by stimulating tRNA aminoacylation, protein synthesis, and tumor cell growth independent of its methyltransferase activity.
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Registered trials
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.