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Acrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.

DC Field Value Language
dc.contributor.authorYang, ES-
dc.contributor.authorWoo, SM-
dc.contributor.authorChoi, KS-
dc.contributor.authorKwon, TK-
dc.date.accessioned2012-04-24T05:33:30Z-
dc.date.available2012-04-24T05:33:30Z-
dc.date.issued2011-
dc.identifier.issn0014-4827-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/6536-
dc.description.abstractTRAIL resistance in many cancer cells is one of the major problems in TRAIL-based cancer therapy. Thus, the agents that can sensitize the tumor cells to TRAIL-mediated apoptosis are strictly needed for the improvement of anti-cancer effect of TRAIL. Acrolein is a byproduct of lipid peroxidation, which has been involved in pulmonary, cardiac and neurodegenerative diseases. We investigated whether acrolein, an α,β-unsaturated aldehyde, can potentiate TRAIL-induced apoptosis in human renal cancer cells. The combined treatment with acrolein and TRAIL significantly induced apoptosis, and stimulated of caspase-3 activity, DNA fragmentation, and cleavage of PARP. We found that acrolein down-regulated the protein level of Bcl-2 and Bcl-2 overexpression inhibited the cell death induced by the combined treatment with acrolein and TRAIL. In addition, acrolein up-regulated C/EBP homologous protein (CHOP) and TRAIL death receptor 5 (DR5) and down-regulation of CHOP or DR5 expression using the respective small interfering RNA significantly attenuated the apoptosis induced by acrolein plus TRAIL. Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL. Taken together, our results demonstrated that acrolein enhances TRAIL-induced apoptosis in Caki cells through down-regulation of Bcl-2 and ROS dependent up-regulation of DR5.-
dc.language.isoen-
dc.subject.MESHAcrolein/*pharmacology-
dc.subject.MESHApoptosis/*drug effects-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHDown-Regulation/drug effects-
dc.subject.MESHGene Expression Regulation/*drug effects-
dc.subject.MESHHumans-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2/*metabolism-
dc.subject.MESHReactive Oxygen Species/*metabolism-
dc.subject.MESHReceptors, TNF-Related Apoptosis-Inducing Ligand/*metabolism-
dc.subject.MESHRecombinant Proteins/metabolism-
dc.subject.MESHStructure-Activity Relationship-
dc.subject.MESHTNF-Related Apoptosis-Inducing Ligand/*metabolism-
dc.subject.MESHTumor Cells, Cultured-
dc.subject.MESHUp-Regulation/drug effects-
dc.titleAcrolein sensitizes human renal cancer Caki cells to TRAIL-induced apoptosis via ROS-mediated up-regulation of death receptor-5 (DR5) and down-regulation of Bcl-2.-
dc.typeArticle-
dc.identifier.pmid21854768-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0014-4827(11)00328-4-
dc.contributor.affiliatedAuthor최, 경숙-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.yexcr.2011.08.005-
dc.citation.titleExperimental cell research-
dc.citation.volume317-
dc.citation.number18-
dc.citation.date2011-
dc.citation.startPage2592-
dc.citation.endPage2601-
dc.identifier.bibliographicCitationExperimental cell research, 317(18):2592-2601, 2011-
dc.identifier.eissn1090-2422-
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Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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