| Different G2/M accumulation in M059J and M059K cells after exposure to DNA double-strand break-inducing agents. | |
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MedLine Citation:
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PMID: 15708275 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: To investigate and compare the cell cycle progression in relation to cell death in the human glioma cell lines, M059J and M059K, after exposure to DNA double-strand break-inducing agents. METHODS AND MATERIALS: The M059J and M059K cells, deficient and proficient in the catalytic subunit of the DNA-dependent protein kinase, respectively, were exposed to 1 and 4 Gy of photons or accelerated nitrogen ions. In addition, M059J and M059K cells were treated with 10 and 40 mug/mL of bleomycin for 30 min, respectively. Cell cycle progression, monitored by DNA flow cytometry, was measured up to 72 h after treatment. RESULTS: M059J, but not M059K, cells displayed G(2)/M accumulation after low linear energy transfer irradiation. High linear energy transfer radiation exposure however, resulted in a substantial increase of M059K cells in the G(2)/M phase detected at 48 h. At 72 h, the number of cells in the G(2)/M phase was equivalent to its control. M059J cells accumulated mainly in S phase after high linear energy transfer irradiation. In contrast to M059K, M059J cells were still blocked at 72 h. Bleomycin induced G(2)/M accumulation for both M059J and M059K cells detected 24 h after treatment. At 48 h, the percentage of bleomycin-treated M059J cells in G(2)/M phase remained high, and the number of M059K cells had decreased to control levels. Neither cell line showed cell cycle arrest (< or =10 h) after exposure to these agents. CONCLUSION: Distinct cell cycle block and release is dependent on the complexity of the induced DNA damage and the presence of the DNA-dependent protein kinase catalytic subunit. |
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Authors:
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Asa Holgersson; Thomas Heiden; Juan Castro; Margareta R Edgren; Rolf Lewensohn; Annelie E Meijer |
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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 radiation oncology, biology, physics Volume: 61 ISSN: 0360-3016 ISO Abbreviation: Int. J. Radiat. Oncol. Biol. Phys. Publication Date: 2005 Mar |
Date Detail:
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Created Date: 2005-02-14 Completed Date: 2005-03-24 Revised Date: 2012-06-25 |
Medline Journal Info:
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Nlm Unique ID: 7603616 Medline TA: Int J Radiat Oncol Biol Phys Country: United States |
Other Details:
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Languages: eng Pagination: 915-21 Citation Subset: IM |
Affiliation:
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Department of Oncology-Pathology, Unit of Medical Radiation Biology, Karolinska Institutet, SE-171 76 Stockholm, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antimetabolites, Antineoplastic
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pharmacology Bleomycin / pharmacology Cell Cycle / drug effects, physiology, radiation effects* DNA Damage* DNA Repair DNA-Activated Protein Kinase DNA-Binding Proteins / metabolism G2 Phase / physiology Glioma / metabolism, pathology* Humans Linear Energy Transfer Mitosis / physiology Nuclear Proteins Protein-Serine-Threonine Kinases / metabolism Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Antimetabolites, Antineoplastic; 0/DNA-Binding Proteins; 0/Nuclear Proteins; 11056-06-7/Bleomycin; EC 2.7.11.1/DNA-Activated Protein Kinase; EC 2.7.11.1/PRKDC protein, human; EC 2.7.11.1/Protein-Serine-Threonine Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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