| A G2/M growth arrest response to low-dose intermittent H2O2 in normal uroepithelial cells. | |
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MedLine Citation:
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PMID: 10938379 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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M Chien; C Rinker-Schaeffer; W M Stadler |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of oncology Volume: 17 ISSN: 1019-6439 ISO Abbreviation: Int. J. Oncol. Publication Date: 2000 Sep |
Date Detail:
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Created Date: 2000-11-20 Completed Date: 2000-11-20 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9306042 Medline TA: Int J Oncol Country: GREECE |
Other Details:
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Languages: eng Pagination: 425-32 Citation Subset: IM |
Affiliation:
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Sections of Urology and Hematology/Oncology, Departments of Surgery and Medicine, Prostate Cancer Program, Cancer Research Center, University of Chicago, IL 60637, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis 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 Humans Hydrogen Peroxide / administration & dosage, pharmacology* Metaphase / drug effects* Nuclear Proteins* Oxidative Stress Papillomaviridae / physiology Phosphorylation 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 |
| Chemical | |
Reg. No./Substance:
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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 2.7.11.22/Cyclin-Dependent Kinases; EC 3.2.1.23/beta-Galactosidase; EC 6.3.2.19/MDM2 protein, human; EC 6.3.2.19/Proto-Oncogene Proteins c-mdm2 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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