ArticleCell cycle (Georgetown, Tex.)2015
Nucleolar repression facilitates initiation and maintenance of senescence.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Tumor cells escape from therapy-induced senescence: from molecular mechanisms to targeted intervention.Biology direct · 2026Review
- EIF1AX Nucleolar Condensates Enhance Susceptibilities for the Management of Endometrial Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nucleolar expansion: A biomolecular condensate mortality timer.Geromedicine · 2026Article
- Pan-cancer analysis of m1A writer gene RRP8: implications for immune infiltration and prognosis in human cancers.Discover oncology · 2024Article
- PQBP3 prevents senescence by suppressing PSME3-mediated proteasomal Lamin B1 degradation.The EMBO journal · 2024Article
- Peripheral Blood Gene Expression Profiling Reveals Molecular Pathways Associated with Cervical Artery Dissection.International journal of molecular sciences · 2024Article
- RRP8, associated with immune infiltration, is a prospective therapeutic target in hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2024Article
- Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseases.The Journal of clinical investigation · 2023Article
- Cellular senescence and abdominal aortic aneurysm: From pathogenesis to therapeutics.Frontiers in cardiovascular medicine · 2022Review
- The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Antagonising Chromatin Remodelling Activities in the Regulation of Mammalian Ribosomal Transcription.Genes · 2021Review
- Targeting cellular senescence based on interorganelle communication, multilevel proteostasis, and metabolic control.The FEBS journal · 2021Review
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- MeCP2 facilitates breast cancer growth via promoting ubiquitination-mediated P53 degradation by inhibiting RPL5/RPL11 transcription.Oncogenesis · 2020Article
- Estrogen Signaling Induces Mitochondrial Dysfunction-Associated Autophagy and Senescence in Breast Cancer Cells.Biology · 2020Article
- Senescence-Associated Pro-inflammatory Cytokines and Tumor Cell Plasticity.Frontiers in molecular biosciences · 2020Review
- GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2019Article
- Inhibition of nucleolar stress response by Sirt1: A potential mechanism of acetylation-independent regulation of p53 accumulation.Aging cell · 2019Article
- Various Nucleolar Stress Inducers Result in Highly Distinct Changes in Water, Dry Mass and Elemental Content in Cancerous Cell Compartments: Investigation Using a Nano-Analytical Approach.Nanotheranostics · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor cells with defective apoptosis pathways often respond to chemotherapy by entering irreversible cell cycle arrest with features of senescence. However, rare cells can bypass entry to senescence, or re-enter cell cycle from a senescent state. Deficiency in senescence induction and maintenance may contribute to treatment resistance and early relapse after therapy. Senescence involves epigenetic silencing of cell cycle genes and reduced rRNA transcription. We found that senescence-inducing treatments such as DNA damage and RNA polymerase I inhibition stimulate the binding between the nucleolar protein NML (nucleomethylin) and SirT1. The NML complex promotes rDNA heterochromatin formation and represses rRNA transcription. Depletion of NML reduced the levels of H3K9Me3 and H3K27Me3 heterochromatin markers on rDNA and E2F1 target promoters in senescent cells, increased rRNA transcription, and increased the frequency of cell cycle re-entry. Depletion of the nucleolar transcription repressor factor TIP5 also promoted escape from senescence. Furthermore, tumor tissue staining showed that breast tumors without detectable nucleolar NML expression had poor survival. The results suggest that efficient regulation of nucleolar rDNA transcription facilitates the maintenance of irreversible cell cycle arrest in senescent cells. Deficiency in nucleolar transcription repression may accelerate tumor relapse after chemotherapy.
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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.