ArticleOncogene2016
Caspases uncouple p27(Kip1) from cell cycle regulated degradation and abolish its ability to stimulate cell migration and invasion.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- The Role of Caspases in Melanoma Pathogenesis.Current issues in molecular biology · 2024Review
- Review
- A Truncated Form of the p27 Cyclin-Dependent Kinase Inhibitor Translated from Pre-mRNA Causes GMolecular and cellular biology · 2022Article
- The SKP2-p27 axis defines susceptibility to cell death upon CHK1 inhibition.Molecular oncology · 2022Article
- Xeroderma Pigmentosum: General Aspects and Management.Journal of personalized medicine · 2021Review
- Stimulation of ROS Generation by Extract ofAntioxidants (Basel, Switzerland) · 2021Article
- Cell cycle-dependent active stress drives epithelia remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A New CYP2E1 Inhibitor, 12-Imidazolyl-1-dodecanol, Represents a Potential Treatment for Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2021Article
- Cell Cycle Deficits in Neurodegenerative Disorders: Uncovering Molecular Mechanisms to Drive Innovative Therapeutic Development.Aging and disease · 2020Review
- Cell-Cycle Cross Talk with Caspases and Their Substrates.Cold Spring Harbor perspectives in biology · 2020Review
- Caspase-8-dependent control of NK- and T cell responses during cytomegalovirus infection.Medical microbiology and immunology · 2019Review
- p27/Kip1 functions as a tumor suppressor and oncoprotein in osteosarcoma.Scientific reports · 2019Article
- Rottlerin promotes autophagy and apoptosis in gastric cancer cell lines.Molecular medicine reports · 2018Article
- Mapping Interactions between p27 and RhoA that Stimulate Cell Migration.Journal of molecular biology · 2018Article
- Perturbing mitosis for anti-cancer therapy: is cell death the only answer?EMBO reports · 2018Review
- Transcriptome Analysis of Gene Expression Provides New Insights into the Effect of Mild Therapeutic Hypothermia on Primary Human Cortical Astrocytes Cultured under Hypoxia.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
In addition to their role in programmed cell death, caspases exert non-lethal functions in diverse developmental processes including cell differentiation or tissue remodeling. Terminal cell cycle exit and differentiation can be promoted by increased level of the CDK inhibitor p27(Kip1). Activated caspases cause proteolytic processing of p27, and we identified a novel caspase cleavage site in human p27 that removes a C-terminal fragment of 22 amino acids from the CDK inhibitor, including a phosphodegron. Thereby, caspases protect the inhibitor from SCF-Skp2-mediated degradation in S, G2 and M phases of the cell cycle. As a consequence, p27 becomes stabilized and remains an efficient nuclear inhibitor of cell cycle progression. Besides controlling cyclin/CDK kinase activity, p27 also regulates cytoskeletal dynamics, cell motility and cell invasion. Following processing by caspases, p27 fails to bind to RhoA and to inhibit its activation, and thereby abolishes the ability of p27 to stimulate cell migration and invasion. We propose that the stabilization of the CDK inhibitor and elimination of RhoA-induced cytoskeletal remodeling upon caspase processing could contribute to cell cycle exit and cytoskeletal remodeling during non-lethal caspase controlled differentiation processes.
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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.