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dc.contributor.authorDong, Lan-fengen_US
dc.contributor.authorLambrechts, Ruthen_US
dc.contributor.authorLiu, Jien_US
dc.contributor.authorZobalova, Renataen_US
dc.contributor.authorMarin-Hernandez, Alvaroen_US
dc.contributor.authorStantic, Marinaen_US
dc.contributor.authorRohlena, Jakuben_US
dc.contributor.authorValis, Karelen_US
dc.contributor.authorRodriguez-Enriquez, Saraen_US
dc.contributor.authorButcher, Bevanen_US
dc.contributor.authorGoodwin, Jacoben_US
dc.contributor.authorT. Brunk, Ulfen_US
dc.contributor.authorK. Witting, Paulen_US
dc.contributor.authorMoreno-Sanchez, Rafaelen_US
dc.contributor.authorE. Scheffler, Immoen_US
dc.contributor.authorRalph, Stephenen_US
dc.contributor.authorNeuzil, Jirien_US
dc.date.accessioned2017-05-03T15:05:20Z
dc.date.available2017-05-03T15:05:20Z
dc.date.issued2009en_US
dc.date.modified2010-06-07T08:05:53Z
dc.identifier.issn10780432en_US
dc.identifier.doi10.1158/1078-0432.CCR-08-2439en_AU
dc.identifier.urihttp://hdl.handle.net/10072/30091
dc.description.abstractPurpose: Vitamin E analogues are potent novel anticancer drugs. The purpose of this study was to elucidate the cellular target by which these agents, represented by a-tocopoheryl succinate (a-TOS), suppress tumors in vivo, with the focus on the mitochondrial complex II (CII). Experimental Design: Chinese hamster lung fibroblasts with functional, dysfunctional, and reconstituted CII were transformed using H-Ras. The cells were then used to form xenografts in immunocompromized mice, and response of the cells and the tumors to a-TOS was studied. Results: The CII-functional and CII-reconstituted cells, unlike their CII-dysfunctional counterparts, responded to a-TOS by reactive oxygen species generation and apoptosis execution. Tumors derived from these cell lines reciprocated their responses to a-TOS. Thus, growth of CII-functional and CII-reconstituted tumors was strongly suppressed by the agent, and this was accompanied by high level of apoptosis induction in the tumor cells. On the other hand, a-TOS did not inhibit the CII-dysfuntional tumors. Conclusions: We document in this report a novel paradigm, according to which the mitochondrial CII, which rarely mutates in human neoplasias, is a plausible target for anticancer drugs from the group of vitamin E analogues, providing support for their testing in clinical trials.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.format.extent111326 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherAmerican Association for Cancer Researchen_US
dc.publisher.placeUSAen_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom1593en_US
dc.relation.ispartofpageto1600en_US
dc.relation.ispartofissue5en_US
dc.relation.ispartofjournalClinical Cancer Researchen_US
dc.relation.ispartofvolume15en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchMolecular Targetsen_US
dc.subject.fieldofresearchcode111207en_US
dc.titleSuppression of Tumor Growth In vivo by the Mitocan α-tocopheryl Succinate Requires Respiratory Complex IIen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.rights.copyrightCopyright 2009 AACR. This is the author-manuscript version of the paper. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal link for access to the definitive, published version.en_AU
gro.date.issued2009
gro.hasfulltextFull Text


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