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

Title
Helenalin-induced apoptosis is dependent on production of reactive oxygen species and independent of induction of endoplasmic reticulum stress in renal cell carcinoma
Author(s)
이태진장지훈[장지훈]Taha Iqbal[Taha Iqbal]민경진[민경진]김신[김신]박종욱[박종욱]손은익[손은익]권택규[권택규]
Keywords
UNFOLDED PROTEIN RESPONSE; SESQUITERPENE LACTONES; NEURODEGENERATIVE DISEASES; CANCER CELLS; DEATH; EXPRESSION; AGENTS; ATF4; INHIBITION; MECHANISMS
Issue Date
201303
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Citation
TOXICOLOGY IN VITRO, v.27, no.2, pp.588 - 596
Abstract
Helenalin, a sesquiterpene lactone, exhibits anti-inflammatory and anti-tumor activities. Here, we investigated 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 carcinoma 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 regulated 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. (C) 2012 Elsevier Ltd. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/26265http://dx.doi.org/10.1016/j.tiv.2012.10.014
ISSN
0887-2333
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의과대학 > 해부학교실 > Articles
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