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Article: The Kappa-opioid receptor specific agonist U50488H induces mitochondrial stress in cultured human cancer cells

TitleThe Kappa-opioid receptor specific agonist U50488H induces mitochondrial stress in cultured human cancer cells
Authors
Issue Date2005
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJB
Citation
The F E B S Journal, 2005, v. 272 Supplement 1, p. 61, Abstract no. n5-029p How to Cite?
AbstractIn this study, the cell death that was induced by a specific agonist of kappa-opioid receptor, U50488H, was investigated in a cultured human cell line (CNE2). A loss of cellular viability and a decrease of cell number were observed when cells were treated for twenty-four hours with U50488H (50–100 lm). Examination of these treated cells by electron microscopy demonstrated swelling of mitochondria without much evidence of chromosomal fragmentation. Consistently, the presence of a sub-G1 peak that was due to DNA-fragmentation was also only found in cells treated with staurosporine (serving as an apoptotic stimulus) but not U50488H. Only a small fraction of procaspase-3 had undergone limited proteolysis when cells were treated with U50488H. However, the uptake of the mitochondrial dye DiOC6 was tremendously reduced in cells treated with U50488H (in comparison to the control) suggesting that dissipation of mitochondrial potential had taken place. The decrease in the uptake of DiOC6 was accompanied by the release of cytochrome-C as shown by immunofluorescence experiments. Incubation of cells with U50488H in the presence of cyclosporine-A was able to prevent the release of cytochrome-C suggesting the involvement of permeability transition. It is proposed that the kappa-opioid receptor specific agonist U50488H might cause a type of cell death that was relatively independent of the activation of procaspase-3, but involving the development of mitochondrial stress as evident by the drop in mitochondrial potential and the release of cytochrome-C.
Persistent Identifierhttp://hdl.handle.net/10722/68152
ISSN
2015 Impact Factor: 4.237
2015 SCImago Journal Rankings: 2.141

 

DC FieldValueLanguage
dc.contributor.authorWong, NSen_HK
dc.contributor.authorPoon, WHen_HK
dc.date.accessioned2010-09-06T06:01:51Z-
dc.date.available2010-09-06T06:01:51Z-
dc.date.issued2005en_HK
dc.identifier.citationThe F E B S Journal, 2005, v. 272 Supplement 1, p. 61, Abstract no. n5-029pen_HK
dc.identifier.issn1742-464Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/68152-
dc.description.abstractIn this study, the cell death that was induced by a specific agonist of kappa-opioid receptor, U50488H, was investigated in a cultured human cell line (CNE2). A loss of cellular viability and a decrease of cell number were observed when cells were treated for twenty-four hours with U50488H (50–100 lm). Examination of these treated cells by electron microscopy demonstrated swelling of mitochondria without much evidence of chromosomal fragmentation. Consistently, the presence of a sub-G1 peak that was due to DNA-fragmentation was also only found in cells treated with staurosporine (serving as an apoptotic stimulus) but not U50488H. Only a small fraction of procaspase-3 had undergone limited proteolysis when cells were treated with U50488H. However, the uptake of the mitochondrial dye DiOC6 was tremendously reduced in cells treated with U50488H (in comparison to the control) suggesting that dissipation of mitochondrial potential had taken place. The decrease in the uptake of DiOC6 was accompanied by the release of cytochrome-C as shown by immunofluorescence experiments. Incubation of cells with U50488H in the presence of cyclosporine-A was able to prevent the release of cytochrome-C suggesting the involvement of permeability transition. It is proposed that the kappa-opioid receptor specific agonist U50488H might cause a type of cell death that was relatively independent of the activation of procaspase-3, but involving the development of mitochondrial stress as evident by the drop in mitochondrial potential and the release of cytochrome-C.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/EJBen_HK
dc.relation.ispartofThe F E B S Journalen_HK
dc.rightsThe F E B S Journal. Copyright © Blackwell Publishing Ltd.en_HK
dc.titleThe Kappa-opioid receptor specific agonist U50488H induces mitochondrial stress in cultured human cancer cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-464X&volume=272 Supplement 1&spage=n5&epage=029p&date=2005&atitle=The+Kappa-opioid+receptor+specific+agonist+U50488H+induces+mitochondrial+stress+in+cultured+human+cancer+cells.en_HK
dc.identifier.emailWong, NS: nswong@hkucc.hku.hken_HK
dc.identifier.emailPoon, WH: janpoon@hkusua.hku.hken_HK
dc.identifier.authorityWong, NS=rp00340en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2005.4739_2.x-
dc.identifier.hkuros114930en_HK

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