ArticleCell cycle (Georgetown, Tex.)2013
A high-content cellular senescence screen identifies candidate tumor suppressors, including EPHA3.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- CK2α Overexpression in Colorectal Cancer: Evidence for Sex- and Age-Linked Differences.Cancers · 2025Article
- Loss of myosin light chain kinase induces the cellular senescence associated secretory phenotype to promote breast epithelial cell migration.Scientific reports · 2024Article
- Identification of Piperidine-3-carboxamide Derivatives Inducing Senescence-like Phenotype with Antimelanoma Activities.ACS medicinal chemistry letters · 2021Article
- Review
- Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span.Annual review of pharmacology and toxicology · 2021Review
- Investigation of the role of tyrosine kinase receptor EPHA3 in colorectal cancer.Scientific reports · 2017Article
- EPHA3 regulates the multidrug resistance of small cell lung cancer via the PI3K/BMX/STAT3 signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- miR-204 downregulates EphB2 in aging mouse hippocampal neurons.Aging cell · 2016Article
- Therapeutic targeting of replicative immortality.Seminars in cancer biology · 2015Review
- Identification of a Selective G1-Phase Benzimidazolone Inhibitor by a Senescence-Targeted Virtual Screen Using Artificial Neural Networks.Neoplasia (New York, N.Y.) · 2015Article
- Cell-based screen for altered nuclear phenotypes reveals senescence progression in polyploid cells after Aurora kinase B inhibition.Molecular biology of the cell · 2015Article
- The putative tumor suppressor gene EphA3 fails to demonstrate a crucial role in murine lung tumorigenesis or morphogenesis.Disease models & mechanisms · 2015Article
- Distinctive Structure of the EphA3/Ephrin-A5 Complex Reveals a Dual Mode of Eph Receptor Interaction for Ephrin-A5.PloS one · 2015Article
- Eph- and ephrin-dependent mechanisms in tumor and stem cell dynamics.Cellular and molecular life sciences : CMLS · 2014Review
- Rapamycin induces pluripotent genes associated with avoidance of replicative senescence.Cell cycle (Georgetown, Tex.) · 2013Article
- Spontaneous cellular senescence and stress response heterogeneity in human vestibular schwannomas.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of a cellular senescence program is a common response to prolonged oncogene activation or tumor suppressor loss, providing a physiological mechanism for tumor suppression in premalignant cells. The link between senescence and tumor suppression supports the hypothesis that a loss-of-function screen measuring bona fide senescence marker activation should identify candidate tumor suppressors. Using a high-content siRNA screening assay for cell morphology and proliferation measures, we identify 12 senescence-regulating kinases and determine their senescence marker signatures, including elevation of senescence-associated β-galactosidase, DNA damage and p53 or p16 (INK4a) expression. Consistent with our hypothesis, SNP array CGH data supports loss of gene copy number of five senescence-suppressing genes across multiple tumor samples. One such candidate is the EPHA3 receptor tyrosine kinase, a gene commonly mutated in human cancer. We demonstrate that selected intracellular EPHA3 tumor-associated point mutations decrease receptor expression level and/or receptor tyrosine kinase (RTK) activity. Our study therefore describes a new strategy to mine for novel candidate tumor suppressors and provides compelling evidence that EPHA3 mutations may promote tumorigenesis only when key senescence-inducing pathways have been inactivated.
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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.