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

DC Field Value Language
dc.contributor.author양경미-
dc.contributor.author김병모-
dc.date.accessioned2015-01-06T16:51:52Z-
dc.date.available2015-01-06T16:51:52Z-
dc.date.issued2014-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/98916-
dc.description.abstractω-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.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAcetylcysteine/pharmacology-
dc.subject.MESHAntineoplastic Agents/pharmacology*-
dc.subject.MESHApoptosis/drug effects-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/drug therapy*-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/metabolism-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/pathology-
dc.subject.MESHCaspase 6/metabolism-
dc.subject.MESHCaspase 9/metabolism-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHEndoplasmic Reticulum Stress/drug effects-
dc.subject.MESHFree Radical Scavengers/pharmacology-
dc.subject.MESHGene Knockdown Techniques-
dc.subject.MESHHumans-
dc.subject.MESHLung Neoplasms/drug therapy*-
dc.subject.MESHLung Neoplasms/metabolism-
dc.subject.MESHLung Neoplasms/pathology-
dc.subject.MESHPoly(ADP-ribose) Polymerases/metabolism-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHTranscription Factor CHOP/antagonists & inhibitors-
dc.subject.MESHTranscription Factor CHOP/genetics-
dc.subject.MESHTranscription Factor CHOP/metabolism-
dc.subject.MESHUndecylenic Acids/pharmacology*-
dc.titleω-Hydroxyundec-9-enoic acid induces apoptosis through ROS-mediated endoplasmic reticulum stress in non-small cell lung cancer cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorKyung Mi Yang-
dc.contributor.googleauthorByeong Mo Kim-
dc.contributor.googleauthorJin-Byung Park-
dc.identifier.doi10.1016/j.bbrc.2014.04.111-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02279-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid24796672-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X14007748-
dc.subject.keywordApoptosis-
dc.subject.keywordEndoplasmic reticulum (ER) stress-
dc.subject.keywordN-Acetyl-l-cysteine (NAC)-
dc.subject.keywordNon-small cell lung cancer (NSCLC)-
dc.subject.keywordReactive oxygen species (ROS)-
dc.subject.keywordω-Hydroxyundec-9-enoic acid (ω-HUA)-
dc.contributor.alternativeNameYang, Kyung Mi-
dc.contributor.affiliatedAuthorYang, Kyung Mi-
dc.rights.accessRightsfree-
dc.citation.volume448-
dc.citation.number3-
dc.citation.startPage267-
dc.citation.endPage273-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.448(3) : 267-273, 2014-
dc.identifier.rimsid53779-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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