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A G2/M growth arrest response to low-dose intermittent H2O2 in normal uroepithelial cells.
MedLine Citation:
PMID:  10938379     Owner:  NLM     Status:  MEDLINE    
Studies in fibroblasts have shown that H2O2, as a model for oxidative damage, leads to a G1 growth arrest phenotypically similar to senescence. These observations as well as the observation that bladder cancer is associated with deletions of CDKN2, a gene important in normal senescence, led us to examine normal urothelial cell response to H2O2. We hypothesized that low dose H2O2 exposure would lead to p16 and/or p14arf mediated senescence. We show that H2O2 leads to endogenous beta-galactosidase expression similar to senescence, but instead of G1 arrest, it leads to G2/M growth arrest without induction of either p16 or p14arf. Lack of p21 induction and a similar G2/M growth arrest in E6 immortalized uroepithelial cells suggests that this response is independent of p53 as well. An increased level of cdc2 tyrosine-15 phosphorylation following H2O2 treatment suggests that the observed growth arrest is mediated by a G2 checkpoint mechanism.
M Chien; C Rinker-Schaeffer; W M Stadler
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  17     ISSN:  1019-6439     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2000 Sep 
Date Detail:
Created Date:  2000-11-20     Completed Date:  2000-11-20     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  GREECE    
Other Details:
Languages:  eng     Pagination:  425-32     Citation Subset:  IM    
Sections of Urology and Hematology/Oncology, Departments of Surgery and Medicine, Prostate Cancer Program, Cancer Research Center, University of Chicago, IL 60637, USA.
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MeSH Terms
Cell Aging / drug effects
Cell Cycle Proteins / biosynthesis*,  genetics
Cell Division / drug effects
Cell Line, Transformed
Cell Transformation, Viral
Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinases / metabolism
Cyclins / metabolism
Drug Administration Schedule
G2 Phase / drug effects*
Genes, Reporter
Genes, p16
Hydrogen Peroxide / administration & dosage,  pharmacology*
Metaphase / drug effects*
Nuclear Proteins*
Oxidative Stress
Papillomaviridae / physiology
Protein Biosynthesis
Protein Processing, Post-Translational
Proteins / genetics
Proto-Oncogene Proteins / physiology
Proto-Oncogene Proteins c-mdm2
Recombinant Fusion Proteins / biosynthesis
Signal Transduction / drug effects
Tumor Suppressor Protein p14ARF
Tumor Suppressor Protein p53 / physiology
Urothelium / cytology,  drug effects*
beta-Galactosidase / biosynthesis
Reg. No./Substance:
0/CDKN1A protein, human; 0/Cell Cycle Proteins; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Nuclear Proteins; 0/Proteins; 0/Proto-Oncogene Proteins; 0/Recombinant Fusion Proteins; 0/Tumor Suppressor Protein p14ARF; 0/Tumor Suppressor Protein p53; 7722-84-1/Hydrogen Peroxide; EC Kinases; EC; EC protein, human; EC Proteins c-mdm2

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

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