ArticleNucleic acids research2020
SENEBLOC, a long non-coding RNA suppresses senescence via p53-dependent and independent mechanisms.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- LINP1 suppresses radiation-induced cellular senescence in keratinocytes by modulating the mTOR-p53 axis.Molecular and cellular biochemistry · 2026Article
- Plasma-derived exosomes from obese knee osteoarthritis aggravate synovitis by promoting cellular senescence of synovial fibroblasts.Journal of orthopaedic translation · 2026Article
- Liuwei Dihuang Prevents Human Umbilical Vein Endothelial Cells SenescenceCombinatorial chemistry & high throughput screening · 2026Article
- Nucleolus as a cornerstone linking proliferation and metabolism to cellular responses to stress: involvement of transcription factors MYC and p53.Frontiers in molecular biosciences · 2026Review
- Reciprocal interactions between lncRNAs and MYC in colorectal cancer: partners in crime.Cell death & disease · 2024Review
- Transcription of endogenous retroviruses in senescent cells contributes to the accumulation of double-stranded RNAs that trigger an anti-viral response that reinforces senescence.Cell death & disease · 2024Article
- PURPL and NEAT1 Long Non-Coding RNAs Are Modulated in Vascular Smooth Muscle Cell Replicative Senescence.Biomedicines · 2023Article
- EnhancedScience advances · 2023Article
- Mid-old cells are a potential target for anti-aging interventions in the elderly.Nature communications · 2023Article
- p53-regulated lncRNAs in cancers: from proliferation and metastasis to therapy.Cancer gene therapy · 2023Review
- Metabolic stress-induced reciprocal loop of long noncoding RNA ZFAS1 and ZEB1 promotes epithelial-mesenchymal transition and metastasis of pancreatic cancer cells.Cancer science · 2023Article
- LncRNA NEAT1 suppresses cellular senescence in hepatocellular carcinoma via KIF11-dependent repression of CDKN2A.Clinical and translational medicine · 2023Article
- Counteracting Immunosenescence-Which Therapeutic Strategies Are Promising?Biomolecules · 2023Review
- p53 Dysregulation in Breast Cancer: Insights on Mutations in theInternational journal of molecular sciences · 2023Article
- The potential role of N6-methyladenosine modification of LncRNAs in contributing to the pathogenesis of chronic glomerulonephritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- The impact of senescence on muscle wasting in chronic kidney disease.Journal of cachexia, sarcopenia and muscle · 2023Article
- MYC function and regulation in physiological perspective.Frontiers in cell and developmental biology · 2023Review
- Emerging Role of Non-Coding RNAs in Senescence.Frontiers in cell and developmental biology · 2022Review
- Senolytics: Eliminating Senescent Cells and Alleviating Intervertebral Disc Degeneration.Frontiers in bioengineering and biotechnology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) have emerged as important biological tuners. Here, we reveal the role of an uncharacterized lncRNA we call SENEBLOC that is expressed by both normal and transformed cells under homeostatic conditions. SENEBLOC was shown to block the induction of cellular senescence through dual mechanisms that converge to repress the expression of p21. SENEBLOC facilitates the association of p53 with MDM2 by acting as a scaffold to promote p53 turnover and decrease p21 transactivation. Alternatively, SENEBLOC was shown to affect epigenetic silencing of the p21 gene promoter through regulation of HDAC5. Thus SENEBLOC drives both p53-dependent and p53-independent mechanisms that contribute to p21 repression. Moreover, SENEBLOC was shown to be involved in both oncogenic and replicative senescence, and from the perspective of senolytic agents we show that the antagonistic actions of rapamycin on senescence are dependent on SENEBLOC expression.
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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.