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20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol induces apoptosis via induction of endoplasmic reticulum stress in human colon cancer cells

Title
20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol induces apoptosis via induction of endoplasmic reticulum stress in human colon cancer cells
Authors
Zhang R.Chung Y.Kim H.S.Kim D.-H.Chang W.Y.Hyun J.W.
Ewha Authors
김희선
SCOPUS Author ID
김희선scopus
Issue Date
2013
Journal Title
Oncology Reports
ISSN
1021-335XJCR Link
Citation
vol. 29, no. 4, pp. 1365 - 1370
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Previously, we reported that 20-O-(β-D-glucopyranosyl)- 20(S)-protopanaxadiol (Compound K, a metabolite of ginseng saponin) induces mitochondria-dependent and caspase-dependent apoptosis in HT-29 human colon cancer cells via the generation of reactive oxygen species. The aim of the present study was to elucidate the mechanism underlying apoptosis induced by Compound K with respect to endoplasmic reticulum (ER) stress in HT-29 cells. In the present study, Compound K induced apoptotic cell death as confirmed by DNA fragmentation and apoptotic sub-G1 cell population. Compound K also induced ER stress as indicated by staining with ER tracker, cytosolic and mitochondrial Ca2+ overloading, phosphorylation of protein-kinase-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor-2a (eIF-2a), phosphorylation of IRE-1, splicing of ER stress-specific X-box transcription factor-1 (XBP-1), cleavage of activating transcription factor-6 (ATF-6), upregulation of glucose-regulated protein-78 (GRP-78/BiP) and CCAAT/enhancer-binding protein-homologous protein (CHOP), and cleavage of caspase-12. Furthermore, downregulation of CHOP expression using siCHOP RNA attenuated Compound K-induced apoptosis. Taken together, these results support the important role of ER stress response in mediating Compound K-induced apoptosis in human colon cancer cells. © 2013 Spandidos Publications Ltd. All rights reserved.
DOI
10.3892/or.2013.2270
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의과대학 > 의학과 > Journal papers
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