ArticleMolecular and cellular biology2001
Requirement for p27(KIP1) in retinoblastoma protein-mediated senescence.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 168 citations in OpenAlex.
- Upregulation of CSN8 induces a unique senescence-like state with robust tumor-promoting properties in epithelial ovarian cancer cells under hypoxia.Journal of translational medicine · 2026Article
- Exploring Multi-Target Therapeutic Strategies for Glioblastoma via Endogenous Network Modeling.International journal of molecular sciences · 2025Article
- Review
- Friend or Foe: Regulation, Downstream Effectors of RRAD in Cancer.Biomolecules · 2023Review
- Insights into the role of senescence in tumor dormancy: mechanisms and applications.Cancer metastasis reviews · 2023Review
- Genetic Drivers of Ileal Neuroendocrine Tumors.Cancers · 2021Review
- RAS specific protease induces irreversible growth arrest via p27 in several KRAS mutant colorectal cancer cell lines.Scientific reports · 2021Article
- Ribosomal L1 domain-containing protein 1 coordinates with HDM2 to negatively regulate p53 in human colorectal Cancer cells.Journal of experimental & clinical cancer research : CR · 2021Article
- SENEBLOC, a long non-coding RNA suppresses senescence via p53-dependent and independent mechanisms.Nucleic acids research · 2020Article
- Deubiquitinase PSMD7 regulates cell fate and is associated with disease progression in breast cancer.American journal of translational research · 2020Article
- Convergence of therapy-induced senescence (TIS) and EMT in multistep carcinogenesis: current opinions and emerging perspectives.Cell death discovery · 2020Review
- E2F1 inhibition mediates cell death of metastatic melanoma.Cell death & disease · 2018Article
- Low p16The Prostate · 2017Article
- Interchangeable Roles for E2F Transcriptional Repression by the Retinoblastoma Protein and p27KIP1-Cyclin-Dependent Kinase Regulation in Cell Cycle Control and Tumor Suppression.Molecular and cellular biology · 2017Article
- Senescence and tumor suppression.F1000Research · 2017Review
- Multiple molecular interactions redundantly contribute to RB-mediated cell cycle control.Cell division · 2017Article
- Glioblastoma, hypoxia and autophagy: a survival-prone 'ménage-à-trois'.Cell death & disease · 2016Review
- Article
- Stromal-Initiated Changes in the Bone Promote Metastatic Niche Development.Cell reports · 2016Article
- Conserved Senescence Associated Genes and Pathways in Primary Human Fibroblasts Detected by RNA-Seq.PloS one · 2016Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vivo and in vitro evidence indicate that cells do not divide indefinitely but instead stop growing and undergo a process termed cellular proliferative senescence. Very little is known about how senescence occurs, but there are several indications that the retinoblastoma protein (pRb) is involved, the most striking being that reintroduction of RB into RB(-/-) tumor cell lines induces senescence. In investigating the mechanism by which pRb induces senescence, we have found that pRb causes a posttranscriptional accumulation of the cyclin-dependent kinase inhibitor p27(KIP1) that is accompanied by an increase in p27(KIP1) specifically bound to cyclin E and a concomitant decrease in cyclin E-associated kinase activity. In contrast, pRb-related proteins p107 and p130, which also decrease cyclin E-kinase activity, do not cause an accumulation of p27(KIP1) and induce senescence poorly. In addition, the use of pRb proteins mutated in the pocket domain demonstrates that pRb upregulation of p27(KIP1) and senescence induction do not require the interaction of pRb with E2F. Furthermore, ectopic expression of p21(CIP1) or p27(KIP1) induces senescence but not the morphology change associated with pRb-mediated senescence, uncoupling senescence from the morphological transformation. Finally, the ability of pRb to maintain cell cycle arrest and induce senescence is reversibly abrogated by ablation of p27(KIP1) expression. These findings suggest that prolonged cell cycle arrest through the persistent and specific inhibition of cdk2 activity by p27(KIP1) is critical for pRb-induced senescence.
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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.