ArticleScientific reports2020
N-myristoyltransferase-1 is necessary for lysosomal degradation and mTORC1 activation in cancer cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Epithelial membrane protein 1 in human cancer: a potential diagnostic biomarker and therapeutic target.Biomarkers in medicine · 2024Pooled it
- Lysosomal phosphoinositide turnover acts upstream of RagGTPase-mTORC1 and controls muscle growth.Nature metabolism · 2026Article
- Post-translational modifications at the crossroads of cancer metabolism and immune regulation: therapeutic opportunities and challenges.International journal of surgery (London, England) · 2026Review
- Elevated co-expression of TIMM17A and NMT1 is associated with poor survival in non-small cell lung cancer.Scientific reports · 2025Article
- Inhibition of human N myristoyltransferase 1 as a strategy to suppress cancer progression driven by myristoylation.Scientific reports · 2025Article
- Mechanism of cotranslational protein N-myristoylation in human cells.Molecular cell · 2025Article
- Elucidating the role of N-myristoylation in the excessive membrane localization of PD-L1 in hypoxic cancers and developing a novel NMT1 inhibitor for combination with immune checkpoint blockade therapy.Journal of experimental & clinical cancer research : CR · 2025Article
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- HIV-1 N-myristoylation-dependent hijacking of late endosomes/lysosomes to drive Gag assembly in macrophages.Journal of cell science · 2024Article
- LAMTOR1 ablation impedes cGAS degradation caused by chemotherapy and promotes antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Regulation of autophagy by protein lipidation.Advanced biotechnology · 2024Review
- N-Myristoytransferase Inhibition Causes Mitochondrial Iron Overload and Parthanatos in TIM17A-Dependent Aggressive Lung Carcinoma.Cancer research communications · 2024Article
- Protein lipidation in cancer: mechanisms, dysregulation and emerging drug targets.Nature reviews. Cancer · 2024Review
- Genetic imputation of kidney transcriptome, proteome and multi-omics illuminates new blood pressure and hypertension targets.Nature communications · 2024Article
- The role of N-myristoyltransferase 1 in tumour development.Annals of medicine · 2023Review
- The Ragulator complex: delving its multifunctional impact on metabolism and beyond.Inflammation and regeneration · 2023Review
- The 'omics of obesity in B-cell acute lymphoblastic leukemia.Journal of the National Cancer Institute. Monographs · 2023Article
- Investigating the shared genetic architecture and causal relationship between pain and neuropsychiatric disorders.Human genetics · 2023Article
- SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway.Canadian journal of gastroenterology & hepatology · 2023Article
- Protein acylation: mechanisms, biological functions and therapeutic targets.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
N-myristoyltransferase-1 (NMT1) catalyzes protein myristoylation, a lipid modification that is elevated in cancer cells. NMT1 sustains proliferation and/or survival of cancer cells through mechanisms that are not completely understood. We used genetic and pharmacological inhibition of NMT1 to further dissect the role of this enzyme in cancer, and found an unexpected essential role for NMT1 at promoting lysosomal metabolic functions. Lysosomes mediate enzymatic degradation of vesicle cargo, and also serve as functional platforms for mTORC1 activation. We show that NMT1 is required for both lysosomal functions in cancer cells. Inhibition of NMT1 impaired lysosomal degradation leading to autophagy flux blockade, and simultaneously caused the dissociation of mTOR from the surface of lysosomes leading to decreased mTORC1 activation. The regulation of lysosomal metabolic functions by NMT1 was largely mediated through the lysosomal adaptor LAMTOR1. Accordingly, genetic targeting of LAMTOR1 recapitulated most of the lysosomal defects of targeting NMT1, including defective lysosomal degradation. Pharmacological inhibition of NMT1 reduced tumor growth, and tumors from treated animals had increased apoptosis and displayed markers of lysosomal dysfunction. Our findings suggest that compounds targeting NMT1 may have therapeutic benefit in cancer by preventing mTORC1 activation and simultaneously blocking lysosomal degradation, leading to cancer cell death.
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