|A G2/M growth arrest response to low-dose intermittent H2O2 in normal uroepithelial cells.|
|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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|Type: Journal Article; Research Support, Non-U.S. Gov't|
|Title: International journal of oncology Volume: 17 ISSN: 1019-6439 ISO Abbreviation: Int. J. Oncol. Publication Date: 2000 Sep|
|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|
|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.|
|APA/MLA Format Download EndNote Download BibTex|
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*
Hydrogen Peroxide / administration & dosage, pharmacology*
Metaphase / drug effects*
Papillomaviridae / physiology
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
|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 220.127.116.11/Cyclin-Dependent Kinases; EC 18.104.22.168/beta-Galactosidase; EC 22.214.171.124/MDM2 protein, human; EC 126.96.36.199/Proto-Oncogene Proteins c-mdm2|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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