ArticleNucleic acids research2015
The ribonuclease DIS3 promotes let-7 miRNA maturation by degrading the pluripotency factor LIN28B mRNA.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- Identification and prognostic prediction of high-risk multiple myeloma by exosomal microRNA.Frontiers in oncology · 2025Article
- RNA-binding proteins and exoribonucleases modulating miRNA in cancer: the enemy within.Experimental & molecular medicine · 2024Review
- XRN2 suppresses aberrant entry of tRNA trailers into argonaute in humans and Arabidopsis.PLoS genetics · 2023Article
- Review
- Loss of ribonuclease DIS3 hampers genome integrity in myeloma by disrupting DNA:RNA hybrid metabolism.The EMBO journal · 2022Article
- The OTUD6B-LIN28B-MYC axis determines the proliferative state in multiple myeloma.The EMBO journal · 2022Article
- Genome-wide profiling of 5-hydroxymethylcytosines in circulating cell-free DNA reveals population-specific pathways in the development of multiple myeloma.Journal of hematology & oncology · 2022Article
- DIS3 mutations in multiple myeloma impact the transcriptional signature and clinical outcome.Haematologica · 2022Article
- piRNAs Interact with Cold-Shock Domain-Containing RNA Binding Proteins and Regulate Neuronal Gene Expression During Differentiation.Molecular neurobiology · 2022Article
- Analysis of Genetic Alterations in Ocular Adnexal Mucosa-Associated Lymphoid Tissue Lymphoma With Whole-Exome Sequencing.Frontiers in oncology · 2022Article
- Microhomology-mediated end joining drives complex rearrangements and overexpression ofHaematologica · 2020Article
- The RNA Exosome and Human Disease.Methods in molecular biology (Clifton, N.J.) · 2020Review
- Targeting MYC in multiple myeloma.Leukemia · 2018Review
- Oncogenic mechanisms of Lin28 in breast cancer: new functions and therapeutic opportunities.Oncotarget · 2017Review
- Article
- Targeting RNA for processing or destruction by the eukaryotic RNA exosome and its cofactors.Genes & development · 2017Review
- Collaborative Control of Cell Cycle Progression by the RNA Exonuclease Dis3 and Ras Is Conserved Across Species.Genetics · 2016Article
- Regulatory mechanisms of microRNA expression.Journal of translational medicine · 2016Review
- Biogenesis and regulation of the let-7 miRNAs and their functional implications.Protein & cell · 2016Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma, the second most frequent hematologic tumor after lymphomas, is an incurable cancer. Recent sequencing efforts have identified the ribonuclease DIS3 as one of the most frequently mutated genes in this disease. DIS3 represents the catalytic subunit of the exosome, a macromolecular complex central to the processing, maturation and surveillance of various RNAs. miRNAs are an evolutionarily conserved class of small noncoding RNAs, regulating gene expression at post-transcriptional level. Ribonucleases, including Drosha, Dicer and XRN2, are involved in the processing and stability of miRNAs. However, the role of DIS3 on the regulation of miRNAs remains largely unknown. Here we found that DIS3 regulates the levels of the tumor suppressor let-7 miRNAs without affecting other miRNA families. DIS3 facilitates the maturation of let-7 miRNAs by reducing in the cytoplasm the RNA stability of the pluripotency factor LIN28B, a inhibitor of let-7 processing. DIS3 inactivation, through the increase of LIN28B and the reduction of mature let-7, enhances the translation of let-7 targets such as MYC and RAS leading to enhanced tumorigenesis. Our study establishes that the ribonuclease DIS3, targeting LIN28B, sustains the maturation of let-7 miRNAs and suggests the increased translation of critical oncogenes as one of the biological outcomes of DIS3 inactivation.
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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.