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ω-Hydroxyundec-9-enoic acid induces apoptosis through ROS-mediated endoplasmic reticulum stress in non-small cell lung cancer cells

Authors
 Kyung Mi Yang  ;  Byeong Mo Kim  ;  Jin-Byung Park 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.448(3) : 267-273, 2014 
Journal Title
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 
ISSN
 0006-291X 
Issue Date
2014
MeSH
Acetylcysteine/pharmacology ; Antineoplastic Agents/pharmacology* ; Apoptosis/drug effects ; Carcinoma, Non-Small-Cell Lung/drug therapy* ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Caspase 6/metabolism ; Caspase 9/metabolism ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; Free Radical Scavengers/pharmacology ; Gene Knockdown Techniques ; Humans ; Lung Neoplasms/drug therapy* ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Poly(ADP-ribose) Polymerases/metabolism ; Reactive Oxygen Species/metabolism ; Transcription Factor CHOP/antagonists & inhibitors ; Transcription Factor CHOP/genetics ; Transcription Factor CHOP/metabolism ; Undecylenic Acids/pharmacology*
Keywords
Apoptosis ; Endoplasmic reticulum (ER) stress ; N-Acetyl-l-cysteine (NAC) ; Non-small cell lung cancer (NSCLC) ; Reactive oxygen species (ROS) ; ω-Hydroxyundec-9-enoic acid (ω-HUA)
Abstract
ω-Hydroxyundec-9-enoic acid (ω-HUA), a hydroxyl unsaturated fatty acid derivative, is involved in the antifungal activity of wild rice (Oryza officinalis). Here, we investigated the anti-cancer activity of ω-HUA on a non-small cell lung cancer (NSCLC) cell line. ω-HUA increased apoptosis and induced cleavages of caspase-6, caspase-9, and poly (ADP-ribose) polymerase (PARP). ω-HUA treatment significantly induced endoplasmic reticulum (ER) stress response. Suppression of CHOP expression and inhibiting ER stress by 4-phenylbutyrate (4-PBA) significantly attenuated the ω-HUA treatment-induced activation of caspase-6, caspase-9, and PARP, and subsequent apoptotic cell death, indicating a role for ER stress in ω-HUA-induced apoptosis. In addition, cells subjected to ω-HUA exhibited significantly increased quantity of reactive oxygen species (ROS), and the ROS scavenger N-acetyl-l-cysteine (NAC) inhibited ω-HUA-induced apoptotic cell death and ER stress signals, indicating a role for ROS in ER stress-mediated apoptosis in ω-HUA-treated cells. Taken together, these results suggest that sequential ROS generation and ER stress activation are critical in ω-HUA treatment-induced apoptosis and that ω-HUA represents a promising candidate for NSCLC treatment.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X14007748
DOI
10.1016/j.bbrc.2014.04.111
Appears in Collections:
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)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/98916
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