ArticleEMBO molecular medicine2023
Multi-omic profiling reveals an RNA processing rheostat that predisposes to prostate cancer.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Mitochondrial-specific perturbation of Drosophila RNase Z in neurons leads to motor impairments, disrupted learning and neurodegeneration.PLoS genetics · 2025Article
- Ribonucleases in Mendelian disease: Characterization and insight from model organisms.Genes & diseases · 2025Review
- Pan-cancer and multiomics: advanced strategies for diagnosis, prognosis, and therapy in the complex genetic and molecular universe of cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Extracellular Microvesicle MicroRNAs and Imaging Metrics Improve the Detection of Aggressive Prostate Cancer: A Pilot Study.Cancers · 2025Article
- Structural insights into human ELAC2 as a tRNA 3' processing enzyme.Nucleic acids research · 2024Article
- Illuminating mitochondrial translation through mouse models.Human molecular genetics · 2024Review
- Germline status and micronutrient availability regulate a somatic mitochondrial quality control pathway via short-chain fatty acid metabolism.bioRxiv : the preprint server for biology · 2024Article
- AbioRxiv : the preprint server for biology · 2024Article
- ELAC2 is a functional prostate cancer risk allele.Trends in molecular medicine · 2023Article
- Multi-omic profiling reveals an RNA processing rheostat that predisposes to prostate cancer.EMBO molecular medicine · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the most commonly diagnosed malignancy and the third leading cause of cancer deaths. GWAS have identified variants associated with prostate cancer susceptibility; however, mechanistic and functional validation of these mutations is lacking. We used CRISPR-Cas9 genome editing to introduce a missense variant identified in the ELAC2 gene, which encodes a dually localised nuclear and mitochondrial RNA processing enzyme, into the mouse Elac2 gene as well as to generate a prostate-specific knockout of Elac2. These mutations caused enlargement and inflammation of the prostate and nodule formation. The Elac2 variant or knockout mice on the background of the transgenic adenocarcinoma of the mouse prostate (TRAMP) model show that Elac2 mutation with a secondary genetic insult exacerbated the onset and progression of prostate cancer. Multiomic profiling revealed defects in energy metabolism that activated proinflammatory and tumorigenic pathways as a consequence of impaired noncoding RNA processing and reduced protein synthesis. Our physiologically relevant models show that the ELAC2 variant is a predisposing factor for prostate cancer and identify changes that underlie the pathogenesis of this cancer.
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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.