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Rottlerin induces pro-apoptotic endoplasmic reticulum stress through the protein kinase C-δ-independent pathway in human colon cancer cells

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Author(s)
박종욱권택규
Alternative Author(s)
Park, Jong WookKwon, Taeg Kyu
Publication Year
2008
Abstract
Rottlerin, a compound reported to be a PKC
d-selective inhibitor, has been shown to induce growth
arrest or apoptosis of human cancer cell lines. In our study,
rottlerin dose-dependently induced apoptotic cell death in
colon carcinoma cells. Treatment of HT29 human colon
carcinoma cells with rottlerin was found to induce a
number of signature ER stress markers; phosphorylation of
eukaryotic initiation factor-2a (eIF-2a), ER stress-specific
XBP1 splicing, and up-regulation of glucose-regulated
protein (GRP)-78 and CCAAT/enhancer-binding proteinhomologous
protein (CHOP). However, suppression of
PKC d expression by siRNA or overexpression of
WT-PKC d and DN-PKC d did not abrogate the rottlerinmediated
induction of CHOP. These results suggest that
rottlerin induces up-regulation of CHOP via PKC d-independent
pathway. Furthermore, down-regulation of CHOP
expression using CHOP siRNA attenuated rottlerininduced
apoptosis. Taken together, the present study thus
provides strong evidence to support an important role of
ER stress response in mediating the rottlerin-induced
apoptosis.
Keywords Rottlerin Endoplasmic reticulum stress
Apoptosis CHOP Unfolded protein response
Department
Dept. of Immunology (면역학)
Institute for Medical Science (의과학연구소)
Publisher
School of Medicine
Citation
Apoptosis, Vol.13(11) : 1378-1385, 2008
Type
Article
ISSN
1360-8185
DOI
10.1007/s10495-008-0264-z
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35073
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