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Catechin-7-O-xyloside induces apoptosis via endoplasmic reticulum stress and mitochondrial dysfunction in human non-small cell lung carcinoma H1299 cells

 Jang Won Yoon  ;  Jong Suk Lee  ;  Byeong Mo Kim  ;  Joungjwa Ahn  ;  Kyung Mi Yang 
 ONCOLOGY REPORTS, Vol.31(1) : 314-320, 2014 
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Animals ; Apoptosis/drug effects* ; Carcinoma, Non-Small-Cell Lung/enzymology* ; Caspase 6/biosynthesis* ; Catechin/analogs & derivatives* ; Catechin/pharmacology* ; Cell Line, Tumor ; Endoplasmic Reticulum Stress* ; Humans ; L-Lactate Dehydrogenase/secretion ; Lung Neoplasms/enzymology* ; Membrane Potential, Mitochondrial/drug effects ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mitochondria/drug effects* ; Neoplasm Transplantation ; Poly(ADP-ribose) Polymerases/metabolism ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Small Interfering ; Transcription Factor CHOP/biosynthesis ; Transcription Factor CHOP/genetics ; Xylose/analogs & derivatives* ; Xylose/pharmacology
The medicinal plant Ulmus davidiana var. japonica has significant potential as a cancer chemoprevention agent. Catechin-7-O-xyloside (C7Ox) was purified from ultrafine U. davidiana var. japonica ethanol extract. In the present study, we investigated the apoptotic effect of C7Ox in the non-small cell lung cancer (NSCLC) cell line H1299. C7Ox treatment induced cell death and decreased plasma membrane integrity, an event typical of apoptosis. C7Ox-induced apoptosis was associated with the proteolytic activation of caspase-6, cleavage of poly(ADP-ribose) polymerase (PARP) and loss of mitochondrial membrane potential. C7Ox also induced the endoplasmic reticulum (ER) stress-regulated pro-apoptotic transcription factor CHOP. The suppression of CHOP expression significantly decreased C7Ox-induced cell death, LDH leakage and caspase-6 activation. Antitumor effects, evaluated based on protracted tumor regression, were observed when nude-mice bearing H1299 xenografts were treated with C7Ox. C7Ox-induced tumor regression was accompanied by enhanced expression of CHOP mRNA. Our data suggest that C7Ox can trigger mitochondrial-mediated apoptosis, and that ER stress is critical for C7Ox-induced apoptosis in H1299 NSCLC cells.
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1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Byeong Mo(김병모) ORCID logo https://orcid.org/0000-0002-0582-3132
Yang, Kyung Mi(양경미)
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