ArticleMolecular cell2024
FAM86A methylation of eEF2 links mRNA translation elongation to tumorigenesis.
Article in Molecular cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Leveraging learned representations and multitask learning for lysine methylation site discovery.Scientific reports · 2026Article
- Article
- Leveraging learned representations and multitask learning for lysine methylation site discovery.bioRxiv : the preprint server for biology · 2025Article
- SETD2 suppresses tumorigenesis in a KRASeLife · 2025Article
- Dermal papilla cells-conditioned medium attenuates oxidative stress-induced senescence via ferroptosis inhibition.Scientific reports · 2025Article
- SVC112: From Hummingbirds to Head and Neck Cancer.Advances in experimental medicine and biology · 2025Article
- Elongation factor 2 in cancer: a promising therapeutic target in protein translation.Cellular & molecular biology letters · 2024Review
- Closing in on human methylation-the versatile family of seven-β-strand (METTL) methyltransferases.Nucleic acids research · 2024Review
- ITRAQ Based Proteomics Reveals the Potential Mechanism of Placental Injury Induced by Prenatal Stress.International journal of molecular sciences · 2024Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
eEF2 post-translational modifications (PTMs) can profoundly affect mRNA translation dynamics. However, the physiologic function of eEF2K525 trimethylation (eEF2K525me3), a PTM catalyzed by the enzyme FAM86A, is unknown. Here, we find that FAM86A methylation of eEF2 regulates nascent elongation to promote protein synthesis and lung adenocarcinoma (LUAD) pathogenesis. The principal physiologic substrate of FAM86A is eEF2, with K525me3 modeled to facilitate productive eEF2-ribosome engagement during translocation. FAM86A depletion in LUAD cells causes 80S monosome accumulation and mRNA translation inhibition. FAM86A is overexpressed in LUAD and eEF2K525me3 levels increase through advancing LUAD disease stages. FAM86A knockdown attenuates LUAD cell proliferation and suppression of the FAM86A-eEF2K525me3 axis inhibits cancer cell and patient-derived LUAD xenograft growth in vivo. Finally, FAM86A ablation strongly attenuates tumor growth and extends survival in KRAS
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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 Socratic graph.