CDK2 differentially controls normal cell senescence and cancer cell proliferation upon exposure to reactive oxygen species

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Title
CDK2 differentially controls normal cell senescence and cancer cell proliferation upon exposure to reactive oxygen species
Author(s)
Chae Young Hwang; Seung Min LeeSung Sup ParkKi Sun Kwon
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 425, no. 1, pp. 94-99
Publication Year
2012
Abstract
Reactive oxygen species modulate cell fate in a context-dependent manner. Sublethal doses of H 2O 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 2O 2 increased CDK2 activity with no accompanying change in the PCNA level, leading to cell proliferation. A CDK2 inhibitor, CVT-313, prevented H 2O 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.
Keyword
CDK2H 2O 2P21 Cip1PCNAProliferationSenescence
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bbrc.2012.07.059
Type
Article
Appears in Collections:
Division of Research on National Challenges > Aging Research Center > 1. Journal Articles
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