| CDK2 differentially controls normal cell senescence and cancer cell proliferation upon exposure to reactive oxygen species. | |
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MedLine Citation:
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PMID: 22819841 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Reactive oxygen species modulate cell fate in a context-dependent manner. Sublethal doses of H(2)O(2) decreased the level of proliferating cell nuclear antigen (PCNA) in normal cells (including primary human dermal fibroblasts and IMR-90 cells) without affecting cyclin-dependent kinase 2 (CDK2) activity, leading to cell cycle arrest and subsequent senescence. In contrast, exposure of cancer cells (such as HeLa and MCF7 cells) to H(2)O(2) increased CDK2 activity with no accompanying change in the PCNA level, leading to cell proliferation. A CDK2 inhibitor, CVT-313, prevented H(2)O(2)-induced cancer cell proliferation. These results support the notion that the cyclin/CDK2/p21(Cip1)/PCNA complex plays an important role as a regulator of cell fate decisions. |
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Authors:
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Chae Young Hwang; Seung-Min Lee; Sung Sup Park; Ki-Sun Kwon |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-7-19 |
Journal Detail:
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Title: Biochemical and biophysical research communications Volume: - ISSN: 1090-2104 ISO Abbreviation: - Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-7-23 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012. Published by Elsevier Inc. |
Affiliation:
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Laboratory of Cell Signaling, Aging Research Center, Korea Research Institute of Bioscience and Biotechnology, 125 Gwahangno, Yusong, Daejeon 305-806, Korea. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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