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Arsenic trioxide induces Hsp70 expression via reactive oxygen species and JNK pathway in MDA231 cells

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Affiliated Author(s)
박종욱권택규
Alternative Author(s)
Park, Jong WookKwon, Taeg Kyu
Journal Title
Life Science
ISSN
0024-3205
Issued Date
2005
Keyword
Arsenic trioxideHsp70HSF1ROSNACJNK
Abstract
In the present study, we determined the molecular pathways that induce the heat shock proteins (Hsps) after treatment of cells with arsenic trioxide. Administration of arsenic trioxide to MDA231 cells leads to induce Hsp70, which is accompanied by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK).We showed that arsenic trioxide-induced Hsp70 expression was caused by activation of ROS and prevented by the antioxidant N-Acetyl-Cysteine (NAC). SP600125 and dominant-negative SEK suppressed Hsp70 promoterdriven reporter gene expression, suggesting that JNK would be preferentially associated with the protective heat shock response against arsenic trioxide stress. In addition, SP600125, a specific JNK inhibitor, significantly reduced the amount of phosphorylated HSF1 upon administration of arsenic trioxide. It is likely that Hsp70 expression against arsenic trioxide exposure protects cells from oxidative injury and apoptotic cell death by means of JNK activity.
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Young-Ho Kim et al. (2005). Arsenic trioxide induces Hsp70 expression via reactive oxygen species and JNK pathway in MDA231 cells. Life Science, 77(22), 2783–2793. doi: 10.1016/j.lfs.2005.04.024
Type
Article
ISSN
0024-3205
DOI
10.1016/j.lfs.2005.04.024
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/36298
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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