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Differential effects of resveratrol and novel resveratrol derivative, HS-1793, on endoplasmic reticulum stress-mediated apoptosis and Akt inactivation

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Affiliated Author(s)
박종욱권택규배재훈
Alternative Author(s)
Park, Jong WookKwon, Taeg KyuBae, Jae Hoon
Journal Title
International Journal of Oncology
ISSN
1019-6439
Issued Date
2010
Abstract
. Since resveratrol (3,4',5 tri-hydroxystilbene), which
has been shown to inhibit multistage carcinogenesis, is not a
potent cytotoxic compound, several studies were undertaken
to obtain synthetic analogues of resveratrol with potent
activity. We previously reported that a resveratrol derivative
HS-1793 exhibits stronger antitumor effects than resveratrol
in several cancer cell types. The present study was
undertaken to reveal precise mechanism by which HS-1793
induces cell death. The induction of CCAAT/enhancerbinding
protein-homologous protein (CHOP) and glucoseregulated
protein (GRP)-78, and ER stress-specific XBP1
splicing were found in HT29 human colon carcinoma cells
treated with resveratrol. Conversely, these manifestations
were not observed in HT29 cells treated with HS-1793.
Inhibition of caspase-4 activity by z-LEVD-fmk significantly
reduced the induction of apoptosis by resveratrol but
not by HS-1793. These findings suggest that HS-1793,
contrary to resveratrol, does not induce ER stress-mediated
apoptosis. Importantly, we observed that HS-1793 but not
resveratrol decreased phosphorylated Akt level. We also
demonstrated that HS-1793, compared to resveratrol, exerted
more effective apoptosis inducing activity in Akt-activated
cells. Taken together, the stronger antitumor activity of HS-
1793 originates, at least in part, from its ability for Akt
inactivation.
Department
Dept. of Immunology (면역학)
Dept. of Physiology (생리학)
Publisher
School of Medicine
Citation
HEE JUNG UM et al. (2010). Differential effects of resveratrol and novel resveratrol
derivative, HS-1793, on endoplasmic reticulum
stress-mediated apoptosis and Akt inactivation. International Journal of Oncology, 36(4), 1007–1013. doi: 10.3892/ijo_00000581
Type
Article
ISSN
1019-6439
DOI
10.3892/ijo_00000581
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/36003
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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