ArticleEMBO molecular medicine2014
5-azacytidine inhibits nonsense-mediated decay in a MYC-dependent fashion.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed, 68 citations in OpenAlex.
- Nonsense-mediated mRNA decay: friend or foe in cancer biology?Cell communication and signaling : CCS · 2026Review
- 5-Azacytidine incorporation into mRNAs disrupts translation and induces ribosome collisions.bioRxiv : the preprint server for biology · 2026Article
- Hypoxic stress granules trigger immunogenic dormancy in lung cancer.bioRxiv : the preprint server for biology · 2026Article
- TDP-43 dysfunction leads to the accumulation of cryptic transposable element-derived exons, crypTEs, in iPSC derived neurons and ALS/FTD patient tissues.bioRxiv : the preprint server for biology · 2026Article
- mRNA processing in cancer immunotherapy: emerging targets, resistance mechanisms, and therapeutic opportunities.Frontiers in immunology · 2026Review
- LTO1 and YAE1 regulate MHC-I expression via nonsense-mediated RNA decay in tumor cells.Journal for immunotherapy of cancer · 2025Article
- Nonsense-Mediated mRNA Decay: Mechanisms and Recent Implications in Cardiovascular Diseases.Cells · 2025Review
- Interferons and Cytokines Induce Transcriptional Activation of the Long-Interspersed Element-1 in Myeloid Cells from Autoimmune Patients.European journal of immunology · 2025Article
- Identification of nonsense-mediated decay inhibitors that alter the tumor immune landscape.eLife · 2025Article
- Context specific ubiquitin modification of ribosomes regulates translation under oxidative stress.bioRxiv : the preprint server for biology · 2025Article
- Anticodon-edited tRNA enables translational readthrough of COL4A5 premature termination codons.PloS one · 2025Article
- Therapeutic targeting of RNA for neurological and neuromuscular disease.Genes & development · 2024Review
- Human disease-causing mutations result in loss of leiomodin 2 through nonsense-mediated mRNA decay.PLoS genetics · 2024Article
- Use of 2,6-diaminopurine as a potent suppressor of UGA premature stop codons in cystic fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Recoding of Nonsense Mutation as a Pharmacological Strategy.Biomedicines · 2023Review
- Targeting nonsense-mediated RNA decay does not increase progranulin levels in the Grn R493X mouse model of frontotemporal dementia.PloS one · 2023Article
- Inhibiting DNA methylation and RNA editing upregulates immunogenic RNA to transform the tumor microenvironment and prolong survival in ovarian cancer.Journal for immunotherapy of cancer · 2022Article
- A pan-tumor-siRNA aptamer chimera to block nonsense-mediated mRNA decay inflames and suppresses tumor progression.Molecular therapy. Nucleic acids · 2022Article
- Diverse Roles of the Exon Junction Complex Factors in the Cell Cycle, Cancer, and Neurodevelopmental Disorders-Potential for Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Nonsense-mediated RNA decay: an emerging modulator of malignancy.Nature reviews. Cancer · 2022Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonsense-mediated RNA decay (NMD) is an RNA-based quality control mechanism that eliminates transcripts bearing premature translation termination codons (PTC). Approximately, one-third of all inherited disorders and some forms of cancer are caused by nonsense or frame shift mutations that introduce PTCs, and NMD can modulate the clinical phenotype of these diseases. 5-azacytidine is an analogue of the naturally occurring pyrimidine nucleoside cytidine, which is approved for the treatment of myelodysplastic syndrome and myeloid leukemia. Here, we reveal that 5-azacytidine inhibits NMD in a dose-dependent fashion specifically upregulating the expression of both PTC-containing mutant and cellular NMD targets. Moreover, this activity of 5-azacytidine depends on the induction of MYC expression, thus providing a link between the effect of this drug and one of the key cellular pathways that are known to affect NMD activity. Furthermore, the effective concentration of 5-azacytidine in cells corresponds to drug levels used in patients, qualifying 5-azacytidine as a candidate drug that could potentially be repurposed for the treatment of Mendelian and acquired genetic diseases that are caused by PTC mutations.
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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 OpenQuestion graph.