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Article: Comparative proteomic analysis Of indioside d-triggered cell death in HeLa cells

TitleComparative proteomic analysis Of indioside d-triggered cell death in HeLa cells
Authors
KeywordsApoptosis
Death receptors
Indioside d
Mitochondria
Oxidative stress
Issue Date2008
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobs
Citation
Journal Of Proteome Research, 2008, v. 7 n. 5, p. 2050-2058 How to Cite?
AbstractMedicinal plants represent a rich source of cancer drug leads. Indioside D, a furostanol glycoside isolated from Solanum mammosum, was found to possess antiproliferative activity toward a panel of human cancer cell lines. Proteomic analysis of indioside D-treated HeLa cells revealed profound protein changes related to energy production and oxidative stress, suggesting that mitochondria dysfunction plays a role in indioside D-induced apoptosis. Indioside D caused a rapid dissipation of mitochondrial transmembrane potential (Δψ m) and the generation of reactive oxygen species (ROS), leading to the activation of caspase-dependent apoptotic cell death. The Fas death receptor pathway was also activated following indioside D treatment, and triggered the activation of caspase-8 and cleavage of Bid, which also acted through the mitochondrial apoptosis pathway. These results suggest that indioside D induced apoptosis in HeLa cells via both intrinsic and extrinsic cell death pathways. © 2008 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/89230
ISSN
2015 Impact Factor: 4.173
2015 SCImago Journal Rankings: 1.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, CCen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorCheng, KWen_HK
dc.contributor.authorChiu, JFen_HK
dc.contributor.authorHe, QYen_HK
dc.contributor.authorChen, Fen_HK
dc.date.accessioned2010-09-06T09:54:11Z-
dc.date.available2010-09-06T09:54:11Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Proteome Research, 2008, v. 7 n. 5, p. 2050-2058en_HK
dc.identifier.issn1535-3893en_HK
dc.identifier.urihttp://hdl.handle.net/10722/89230-
dc.description.abstractMedicinal plants represent a rich source of cancer drug leads. Indioside D, a furostanol glycoside isolated from Solanum mammosum, was found to possess antiproliferative activity toward a panel of human cancer cell lines. Proteomic analysis of indioside D-treated HeLa cells revealed profound protein changes related to energy production and oxidative stress, suggesting that mitochondria dysfunction plays a role in indioside D-induced apoptosis. Indioside D caused a rapid dissipation of mitochondrial transmembrane potential (Δψ m) and the generation of reactive oxygen species (ROS), leading to the activation of caspase-dependent apoptotic cell death. The Fas death receptor pathway was also activated following indioside D treatment, and triggered the activation of caspase-8 and cleavage of Bid, which also acted through the mitochondrial apoptosis pathway. These results suggest that indioside D induced apoptosis in HeLa cells via both intrinsic and extrinsic cell death pathways. © 2008 American Chemical Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobsen_HK
dc.relation.ispartofJournal of Proteome Researchen_HK
dc.subjectApoptosisen_HK
dc.subjectDeath receptorsen_HK
dc.subjectIndioside den_HK
dc.subjectMitochondriaen_HK
dc.subjectOxidative stressen_HK
dc.titleComparative proteomic analysis Of indioside d-triggered cell death in HeLa cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1535-3893&volume=7&spage=2050&epage=2058&date=2008&atitle=Comparative+proteomic+analysis+of+indioside+D-triggered+cell+death+in+HeLa+cellsen_HK
dc.identifier.emailChen, F: sfchen@hku.hken_HK
dc.identifier.authorityChen, F=rp00672en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1021/pr800019ken_HK
dc.identifier.pmid18376857-
dc.identifier.scopuseid_2-s2.0-52049093030en_HK
dc.identifier.hkuros147702en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52049093030&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue5en_HK
dc.identifier.spage2050en_HK
dc.identifier.epage2058en_HK
dc.identifier.isiWOS:000255520200025-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, CC=35333095100en_HK
dc.identifier.scopusauthoridWang, Y=7601490707en_HK
dc.identifier.scopusauthoridCheng, KW=12141247000en_HK
dc.identifier.scopusauthoridChiu, JF=7201501692en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK
dc.identifier.scopusauthoridChen, F=7404907980en_HK

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