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

Authors
Young-Ho KimEun-Ju ParkSang Tae HanJong-Wook ParkTaeg Kyu Kwon
Department
Dept. of Immunology (면역학)
Issue Date
2005
Citation
Life Science, Vol.77(22) : 2783-2793, 2005
ISSN
0024-3205
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.
Keywords
Arsenic trioxideHsp70HSF1ROSNACJNK
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/36298
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
Keimyung Author(s)
박종욱; 권택규
Full Text
https://www.sciencedirect.com/science/article/pii/S0024320505005382?via%3Dihub
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