ArticleNature communications2024
Massively parallel screen uncovers many rare 3' UTR variants regulating mRNA abundance of cancer driver genes.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Characterizing highly conserved fragments in 3'UTRs via statistical and transfer learning approaches.NAR genomics and bioinformatics · 2026Article
- Deciphering the comprehensive relationship between 5' UTR and 3' UTR sequences with deep learning.Bioinformatics (Oxford, England) · 2026Article
- The Encyclopedia of DNA Elements.bioRxiv : the preprint server for biology · 2026Article
- Post-transcriptional regulatory networks: The dynamic interplay of RNA-binding proteins.The FEBS journal · 2026Review
- keju: powerful and accurate inference in Massively Parallel Reporter Assays.bioRxiv : the preprint server for biology · 2026Article
- Prime Editing Driven Functional Genomics: Bridging Genotype to Phenotype in the Post-Genomic Era.International journal of molecular sciences · 2026Review
- Meta-analysis of genetic regulation of RNA editing in the human brain identifies new genes underlying neurological disease.medRxiv : the preprint server for health sciences · 2025Article
- Genetic variants affecting RNA stability influence complex traits and disease risk.Nature genetics · 2025Article
- mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025Review
- Human Synthetic Biology and Programmable Gene Regulation Control.Annual review of genomics and human genetics · 2025Review
- U-rich elements drive pervasive cryptic splicing in 3' UTR massively parallel reporter assays.Nature communications · 2025Article
- Genetic Regulation of Alternative Polyadenylation Provides Novel Insights into Molecular Mechanisms Underlying Non-small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The quantitative impact of 3'UTRs on gene expression.Nucleic acids research · 2025Article
- Transcriptomic profiling of unmethylated full mutation carriers implicates TET3 in FMR1 CGG repeat expansion methylation dynamics in fragile X syndrome.Journal of neurodevelopmental disorders · 2025Article
- Dissecting cardiovascular disease-associated noncoding genetic variants using human iPSC models.Stem cell reports · 2025Review
- Cytosine-to-uracil RNA editing is upregulated by pro-inflammatory stimulation of myeloid cells.bioRxiv : the preprint server for biology · 2025Article
- Impact of rare non-coding variants on human diseases through alternative polyadenylation outliers.Nature communications · 2025Article
- Regulatory QTLs affecting miRNA-mRNA interactions in cancer: mechanisms, methods, and clinical implications.Frontiers in molecular biosciences · 2025Review
- Genomic landscape of a long-term surviving patient with metastatic cancer of the larynx: a case report.Frontiers in oncology · 2025Article
- Decoding biology with massively parallel reporter assays and machine learning.Genes & development · 2024Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Understanding the function of rare non-coding variants represents a significant challenge. Using MapUTR, a screening method, we studied the function of rare 3' UTR variants affecting mRNA abundance post-transcriptionally. Among 17,301 rare gnomAD variants, an average of 24.5% were functional, with 70% in cancer-related genes, many in critical cancer pathways. This observation motivated an interrogation of 11,929 somatic mutations, uncovering 3928 (33%) functional mutations in 155 cancer driver genes. Functional MapUTR variants were enriched in microRNA- or protein-binding sites and may underlie outlier gene expression in tumors. Further, we introduce untranslated tumor mutational burden (uTMB), a metric reflecting the amount of somatic functional MapUTR variants of a tumor and show its potential in predicting patient survival. Through prime editing, we characterized three variants in cancer-relevant genes (MFN2, FOSL2, and IRAK1), demonstrating their cancer-driving potential. Our study elucidates the function of tens of thousands of non-coding variants, nominates non-coding cancer driver mutations, and demonstrates their potential contributions to cancer.
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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.