ArticleMolecular and cellular biology2010
CENP-A reduction induces a p53-dependent cellular senescence response to protect cells from executing defective mitoses.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 102 citations in OpenAlex.
- FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
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- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- Centromere inactivation during aging can be rescued in human cells.Molecular cell · 2025Article
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- The impact of mosaic loss of the Y chromosome (mLOY) in men of advanced age.Biogerontology · 2024Review
- The role of the dynamic epigenetic landscape in senescence: orchestrating SASP expression.npj aging · 2024Review
- Downregulation of Histone H3.3 Induces p53-Dependent Cellular Senescence in Human Diploid Fibroblasts.Genes · 2024Article
- Loss of the Y Chromosome: A Review of Molecular Mechanisms, Age Inference, and Implications for Men's Health.International journal of molecular sciences · 2024Review
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Investigation of differentially expressed genes related to cellular senescence between high-risk and non-high-risk groups in neuroblastoma.Frontiers in cell and developmental biology · 2024Article
- CRISPR imaging reveals chromatin fluctuation at the centromere region related to cellular senescence.Scientific reports · 2023Article
- Induction of senescence upon loss of the Ash2l core subunit of H3K4 methyltransferase complexes.Nucleic acids research · 2022Article
- Altered polymerase theta expression promotes chromosomal instability in salivary adenoid cystic carcinoma.Journal of cellular and molecular medicine · 2022Article
- The functional impact of nuclear reorganization in cellular senescence.Briefings in functional genomics · 2022Review
- CENP-A Regulation and Cancer.Frontiers in cell and developmental biology · 2022Review
- Breaking the aging epigenetic barrier.Frontiers in cell and developmental biology · 2022Review
- Epigenetic Regulation of Inflammatory Signaling and Inflammation-Induced Cancer.Frontiers in cell and developmental biology · 2022Review
- Recent insights into mechanisms preventing ectopic centromere formation.Open biology · 2021Review
- CENP-A overexpression promotes distinct fates in human cells, depending on p53 status.Communications biology · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an irreversible growth arrest and is presumed to be a natural barrier to tumor development. Like telomere shortening, certain defects in chromosome integrity can trigger senescence; however, the roles of centromere proteins in regulating commitment to the senescent state remains to be established. We examined chromatin structure in senescent human primary fibroblasts and found that CENP-A protein levels are diminished in senescent cells. Senescence-associated reduction of CENP-A is caused by transcriptional and posttranslational control. Surprisingly, forced reduction of CENP-A by short-hairpin RNA was found to cause premature senescence in human primary fibroblasts. This premature senescence is dependent on a tumor suppressor, p53, but not on p16(INK4a)-Rb; the depletion of CENP-A in p53-deficient cells results in aberrant mitosis with chromosome missegregation. We propose that p53-dependent senescence that arises from CENP-A reduction acts as a "self-defense mechanism" to prevent centromere-defective cells from undergoing mitotic proliferation that potentially leads to massive generation of aneuploid cells.
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