| Stress-induced premature senescence (SIPS)--influence of SIPS on radiotherapy. | |
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MedLine Citation:
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PMID: 18219184 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Replicative senescence is a fundamental feature in normal human diploid cells and results from dysfunctional telomeres at the Hayflick cell division limit. Ionizing radiation (IR) prematurely induces the same phenotypes as replicative senescence prior to the Hayflick limit. This process is known as stress-induced premature senescence (SIPS). Since the cell cycle is irreversibly arrested in SIPS-induced cells, even if they are stimulated by various growth factors, it is thought that SIPS is a form of cell death, irreversibly eliminating replicating cells. IR-induced-focus formation of DNA repair proteins, a marker of DNA damage, is detected in SIPS as well as replicative senescent cells. Furthermore, both processes persistently induce cell cycle checkpoint mechanisms, indicating DNA damage created by ionizing radiation induces SIPS in normal cells, possibly by the same mechanisms as those occurring in replicative senescence. Interestingly, IR induces SIPS not only in normal cells, but also in tumor cells. Due to the expression of telomerase in tumor cells, telomere-dependent replicative senescence does not occur. However, SIPS is induced under certain conditions after IR exposure. Thus, cell death triggered by IR can be attributed to apoptosis or SIPS in tumor cells. However, metabolic function remains intact in SIPS-induced cancer cells, and recent studies show that senescence eliminate cells undergoing SIPS secrete various kinds of factors outside the cell, changing the microenvironment. Evidence using co-culture systems containing normal senescent stromal cells and epithelial tumor cells show that factors secreted from senescent stroma cells promote the growth of tumor epithelial cells both in vitro and in vivo. Thus, regulation of factors secreted from SIPS-induced stromal cells, as well as tumor cells, may affect radiotherapy. |
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Authors:
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Masatoshi Suzuki; David A Boothman |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review Date: 2008-01-24 |
Journal Detail:
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Title: Journal of radiation research Volume: 49 ISSN: 0449-3060 ISO Abbreviation: J. Radiat. Res. Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-03-27 Completed Date: 2008-06-10 Revised Date: 2012-03-28 |
Medline Journal Info:
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Nlm Unique ID: 0376611 Medline TA: J Radiat Res Country: Japan |
Other Details:
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Languages: eng Pagination: 105-12 Citation Subset: IM |
Affiliation:
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Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Bystander Effect Cell Aging / physiology, radiation effects* Cells, Cultured Humans Neoplasms / pathology Radiotherapy Stress, Physiological / physiopathology |
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