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Helenalin-induced apoptosis is dependent on production of reactive oxygen species and independent of induction of endoplasmic reticulum stress in renal cell carcinoma

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Author(s)
김신박종욱권택규손은익
Alternative Author(s)
Kim, ShinPark, Jong WookKwon, Taeg KyuSon, Eun Ik
Publication Year
2013
Keyword
HelenalinROSCHOPATF4ApoptosisBcl-2
Abstract
Helenalin, a sesquiterpene lactone, exhibits anti-inflammatory and anti-tumor activities. Here, we inves-
tigated whether helenalin could induce apoptosis in human renal carcinoma Caki cells. Helenalin
increased apoptosis in dose dependent manner in Caki cells, and also induced apoptosis in other carci-
noma cells, such as human renal carcinoma ACHN cells, human colon carcinoma HT29 and HCT116 cells.
We found that helenalin markedly induced endoplasmic reticulum (ER) stress-related genes, such as reg-
ulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 (ATF4)
and/or the CCAAT enhancer-binding protein-homologous protein (CHOP). However, down-regulation of
ATF4 and/or CHOP expression by siRNA had no effect on helenalin-induced apoptosis in Caki and
HCT116 cells. Helenalin increased production of intracellular reactive oxygen species (ROS). Furthermore,
ROS scavengers, N-acetylcystine (NAC), and glutathione ethyl ester (GEE), reduced helenalin-induced
apoptosis. Taken together, helenalin induced apoptosis via ROS generation in human renal carcinoma
Caki cells. Keywords:
Helenalin
ROS
CHOP
ATF4
Apoptosis
Bcl-2
Department
Dept. of Immunology (면역학)
Dept. of Neurosurgery (신경외과학)
Publisher
School of Medicine
Citation
Toxicol In Vitro, Vol.27(2) : 588-596, 2013
Type
Article
ISSN
0887-2333
DOI
10.1016/j.tiv.2012.10.014
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34657
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