ArticleScientific reports2016
Identification of cellular senescence-specific genes by comparative transcriptomics.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 90 citations in OpenAlex.
- Rhenium-Based β-Galactosidase Probe Allows Senescence Profiling by Mass Cytometry.Angewandte Chemie (International ed. in English) · 2026Article
- Therapeutic Immune Reprogramming by Rapamycin Attenuates Plaque Inflammation and Lymphoid Immune Responses in Aged Atherosclerotic Mice.Aging cell · 2026Article
- Karyoptosis mediates cell death and neurodegeneration upon proteotoxic stress.Nature communications · 2026Article
- Crosstalk between TGF-β and Wnt/β-catenin signaling drives fibrogenic and stem-like phenotypes in senescent MDA-MB-231 breast cancer cells.npj aging · 2026Article
- The Microbial Metabolite IDA Sensitizes Tumor Cells to ARF1 Inhibition by Inducing SVIL-dependent Senescence.International journal of biological sciences · 2026Article
- D-amino acid oxidase suppresses hepatocellular carcinoma via oxidizing D-amino acids.Journal of translational medicine · 2025Article
- Imbalanced chromatin distribution in cellular senescence specifies paraspeckle dynamics.Genome biology · 2025Article
- Identification of markers for neurescence through transcriptomic profiling of postmortem human brains.npj aging · 2025Article
- Identification of markers for neurescence through transcriptomic profiling of postmortem human brains.Research square · 2025Article
- Senolytics: charting a new course or enhancing existing anti-tumor therapies?Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Article
- Lysine-specific demethylase 1 (LSD1) suppresses cellular senescence by riboflavin uptake-dependent demethylation activity.Scientific reports · 2025Article
- MicroRNA-34a Mediates the Aldosterone-Induced Acceleration of Endothelial Senescence.International journal of hypertension · 2025Article
- Metformin suppresses esophageal cancer progression through the radiation‑induced cellular senescence of cancer‑associated fibroblasts.Oncology reports · 2024Article
- Proline Dehydrogenase (PRODH) Is Expressed in Lung Adenocarcinoma and Modulates Cell Survival and 3D Growth by Inducing Cellular Senescence.International journal of molecular sciences · 2024Article
- Epigallocatechin gallate (EGCG) modulates senescent endothelial cell-monocyte communication in age-related vascular inflammation.Frontiers in cardiovascular medicine · 2024Article
- Investigating D-Amino Acid Oxidase Expression and Interaction Network Analyses in Pathways Associated With Cellular Stress: Implications in the Biology of Aging.Bioinformatics and biology insights · 2024Article
- Nectin-4 regulates cellular senescence-associated enlargement of cell size.Scientific reports · 2023Article
- Elimination of senescent cells by treatment with Navitoclax/ABT263 reverses whole brain irradiation-induced blood-brain barrier disruption in the mouse brain.GeroScience · 2023Article
- Cancer-specific association between Tau (MAPT) and cellular pathways, clinical outcome, and drug response.Scientific data · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is defined as permanent cell cycle arrest induced by various stresses. Although the p53 transcriptional activity is essential for senescence induction, the downstream genes that are crucial for senescence remain unsolved. Here, by using a developed experimental system in which cellular senescence or apoptosis is induced preferentially by altering concentration of etoposide, a DNA-damaging drug, we compared gene expression profiles of senescent and apoptotic cells by microarray analysis. Subtraction of the expression profile of apoptotic cells identified 20 genes upregulated specifically in senescent cells. Furthermore, 6 out of 20 genes showed p53-dependent upregulation by comparing gene expression between p53-proficient and -deficient cells. These 6 genes were also upregulated during replicative senescence of normal human diploid fibroblasts, suggesting that upregulation of these genes is a general phenomenon in senescence. Among these genes, 2 genes (PRODH and DAO) were found to be directly regulated by p53, and ectopic expression of 4 genes (PRODH, DAO, EPN3, and GPR172B) affected senescence phenotypes induced by etoposide treatment. Collectively, our results identified several proteins as novel downstream effectors of p53-mediated senescence and provided new clues for further research on the complex signalling networks underlying the induction and maintenance of senescence.
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