| Control of senescence by CXCR2 and its ligands. | |
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MedLine Citation:
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PMID: 18838863 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Senescence is an irreversible growth arrest with important physiological implications as it contributes to tumour suppression and may have a role in aging. During senescence, cells suffer profound phenotypic changes affecting amongst others cell morphology and chromatin structure. Senescent cells also undergo significant transcriptional changes, such as the increased production of a plethora of different secreted factors, which are the basis of the so-called senescence-associated secretory phenotype. While some of these factors have been previously shown to possess different pro-tumorigenic activities, we recently demonstrated that the secretion of CXCR2-binding chemokines (such as IL-8 or GROalpha) by senescent cells contribute to reinforce senescence via activation of the p53 pathway. Importantly, our data adds to that presented by several groups suggesting that also other factors secreted during senescence (such as PAI-1, IGFBP-7 or IL-6) contribute to the senescent response. Here, we discuss our findings in the context of the emerging role for secreted factors in regulating senescence through paracrine and/or autocrine mechanisms. |
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Authors:
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Juan C Acosta; Ana O'Loghlen; Ana Banito; Selina Raguz; Jesús Gil |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2008-10-13 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 7 ISSN: 1551-4005 ISO Abbreviation: Cell Cycle Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-10-08 Completed Date: 2008-12-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: United States |
Other Details:
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Languages: eng Pagination: 2956-9 Citation Subset: IM |
Affiliation:
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Cell Proliferation Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, London, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Aging / physiology* Chemokine CXCL1 / metabolism DNA Damage Humans Interleukin-8 / metabolism Ligands Models, Biological Receptors, Interleukin-8B / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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//Cancer Research UK; //Medical Research Council |
| Chemical | |
Reg. No./Substance:
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0/Chemokine CXCL1; 0/Interleukin-8; 0/Ligands; 0/Receptors, Interleukin-8B |
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