Document Detail


Overexpression of cyclin E does not influence homologous recombination in Chinese hamster cells.
MedLine Citation:
PMID:  12163026     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Overexpressed cyclin E in tumours is a prognosticator for poor patient outcome. Cells that overexpress cyclin E have been shown to be impaired in S-phase progression and exhibit genetic instability that may drive this subset of cancers. However, the origin for genetic instability caused by cyclin E overexpression is unknown. Homologous recombination plays an important role in S-phase progression and is also regulated by the same proteins that regulate cyclin E-associated kinase activity, i.e., p53 and p21. To test the hypothesis that overexpressed cyclin E causes genetic instability through homologous recombination, we investigated the effect of cyclin E overexpression on homologous recombination in the hprt gene in a Chinese hamster cell line. Although cyclin E overexpression shortened the G1 phase in the cell cycle as expected, we could see no change in neither spontaneous nor etoposide-induced recombination. Also, overexpression of cyclin E did not affect the repair of DNA double-strand breaks and failed to potentiate the cytotoxic effects of etoposide. Our data suggest that genetic instability caused by overexpression of cyclin E is not mediated by aberrant homologous recombination.
Authors:
Cecilia Lundin; Magnus K R Samuelsson; Thomas Helleday
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  296     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-08-06     Completed Date:  2002-09-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  363-7     Citation Subset:  IM    
Affiliation:
Department of Genetic and Cellular Toxicology, Stockholm University, Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Animals
CHO Cells
Cell Cycle* / drug effects
Cricetinae
Cyclin E / genetics,  metabolism*
DNA / metabolism
DNA Damage
Etoposide / pharmacology
Flow Cytometry
Humans
Nucleic Acid Synthesis Inhibitors / pharmacology
Recombination, Genetic*
Chemical
Reg. No./Substance:
0/Cyclin E; 0/Nucleic Acid Synthesis Inhibitors; 33419-42-0/Etoposide; 9007-49-2/DNA

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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