Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA subpopulations
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| Publicado en: | Nature Communications vol. 16, no. 1 (2025), p. 10460-10475 |
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| Otros Autores: | , , , , , , |
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| Acceso en línea: | Citation/Abstract Full Text Full Text - PDF |
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| 022 | |a 2041-1723 | ||
| 024 | 7 | |a 10.1038/s41467-025-65448-x |2 doi | |
| 035 | |a 3275619782 | ||
| 045 | 2 | |b d20250101 |b d20251231 | |
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| 100 | 1 | |a Zhou, Sihang |u Department of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 245 | 1 | |a Cancer-associated snaR-A noncoding RNA interacts with core splicing machinery and disrupts processing of mRNA subpopulations | |
| 260 | |b Nature Publishing Group |c 2025 | ||
| 513 | |a Journal Article | ||
| 520 | 3 | |a Expansion of RNA polymerase III (Pol III) activity in cancer can activate the transcription of typically silent small RNA genes, including snaR-A (small NF90-associated RNA isoform A), a hominid-specific noncoding RNA that promotes cell proliferation through unclear mechanisms. Here, we show that snaR-A interacts with mRNA splicing factors, including the U2 small nuclear ribonucleoprotein (snRNP) subunit SF3B2, and localizes near subnuclear foci enriched in splicing machinery. Overexpression of snaR-A increases intron retention, a hallmark of inefficient splicing, whereas its depletion enhances splicing of mRNAs characterized by high U2 snRNP occupancy and nuclear speckle proximity. These improvements in splicing coincide with reduced cell proliferation, consistent with tumor-level patterns linking snaR-A to growth in primary cancers. Together, these findings identify snaR-A as a molecular antagonist of splicing and potential disease driver in cancer. We propose that snaR-A-related splicing perturbation may phenocopy splicing defects attributed to U2 snRNP mutations in cancer, eliciting an alternative, non-mutational mechanism of splicing dysregulation during tumorigenesis.Small RNAs such as snaR-A (small NF90-associated RNA isoform A) may contribute to cancer-related phenotypes. Here the authors find that snaR-A interacts with mRNA splicing factors in subnuclear foci and causes splicing defects in mRNA subpopulations, which is associated with increased cell proliferation, and poor outcomes in cancer patients. | |
| 653 | |a Cancer | ||
| 653 | |a Ribonucleoproteins (U2 small nuclear) | ||
| 653 | |a Ontology | ||
| 653 | |a Experiments | ||
| 653 | |a Ribonucleoproteins (small nuclear) | ||
| 653 | |a Ribonucleic acid--RNA | ||
| 653 | |a Phenotypes | ||
| 653 | |a Cell proliferation | ||
| 653 | |a Alternative splicing | ||
| 653 | |a RNA-protein interactions | ||
| 653 | |a Hybridization | ||
| 653 | |a Tumorigenesis | ||
| 653 | |a Splicing factors | ||
| 653 | |a Non-coding RNA | ||
| 653 | |a Localization | ||
| 653 | |a Genes | ||
| 653 | |a Cell growth | ||
| 653 | |a Defects | ||
| 653 | |a DNA-directed RNA polymerase | ||
| 653 | |a Subpopulations | ||
| 653 | |a Environmental | ||
| 700 | 1 | |a Lizarazo, Simon |u Department of Molecular and Integrative Physiology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 700 | 1 | |a Chorghade, Sandip |u Department of Biochemistry, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 700 | 1 | |a Mouli, Leela |u School of Molecular and Cellular Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 700 | 1 | |a Cheng, Ruiying |u Department of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 700 | 1 | |a K C, Rajendra |u Center for Biophysics and Quantitative Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 700 | 1 | |a Kalsotra, Auinash |u Department of Biochemistry, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991); Cancer Center at Illinois, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991); Carl R. Woese Institute for Genomic Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991); Chan Zuckerberg Biohub Chicago, LLC, Chicago, IL, USA | |
| 700 | 1 | |a Van Bortle, Kevin |u Department of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991); Cancer Center at Illinois, University of Illinois Urbana-Champaign, Urbana, IL, USA (ROR: https://ror.org/047426m28) (GRID: grid.35403.31) (ISNI: 0000 0004 1936 9991) | |
| 773 | 0 | |t Nature Communications |g vol. 16, no. 1 (2025), p. 10460-10475 | |
| 786 | 0 | |d ProQuest |t Health & Medical Collection | |
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