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Article: Id-1-induced Raf/MEK pathway activation is essential for its protective role against taxol-induced apoptosis in nasopharyngeal carcinoma cells

TitleId-1-induced Raf/MEK pathway activation is essential for its protective role against taxol-induced apoptosis in nasopharyngeal carcinoma cells
Authors
Issue Date2004
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2004, v. 25 n. 6, p. 881-887 How to Cite?
AbstractIncreasingly, evidence supports the function of the helix-loop-helix protein Id-1 (inhibitor of differentiation/DNA binding-1) as an oncogene. Over-expression of Id-1 is not only observed in many types of human cancer but its expression levels have been correlated with cancer progression. However, little is known about the molecular mechanisms responsible for the function of Id-1. Recently, we and others reported that Id-1-induced cell proliferation was mediated through a Raf/MEK signalling pathway. In this study, we investigated if ectopic Id-1 expression in nasopharyngeal carcinoma cells had any protective effect on taxol-induced death, which is also regulated through Raf/MEK pathway. Using four stable Id-1 transfectant clones, we found that exogenous Id-1 expression led to phosphorylation of Raf-1 and MEK1/2 kinases, which was associated with resistance to taxol. Treatment of the Id-1 expressing cells with a MEK inhibitor, PD098059, resulted in an increased taxol-induced apoptosis rate in Id-1 transfectants compared with the vector control. In addition, the fact that the taxol-induced apoptosis rate, down-regulation of Bcl-2 and up-regulation of Bax were suppressed by PD098059 treatment in Id-1 expressing cells indicates that the Id-1 induced cellular protection against apoptosis is mediated through Raf/MEK signalling pathways. Our results suggest that Id-1 may be an upstream regulator of the Raf/MEK signalling pathway, which plays an essential role in protection against taxol-induced apoptosis. Our evidence also indicates a novel treatment strategy to increase anticancer drug-induced apoptosis through inactivation of the Id-1 protein. © Oxford University Press 2004; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/149646
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, HWen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorWang, Xen_US
dc.date.accessioned2012-06-26T05:56:29Z-
dc.date.available2012-06-26T05:56:29Z-
dc.date.issued2004en_US
dc.identifier.citationCarcinogenesis, 2004, v. 25 n. 6, p. 881-887en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10722/149646-
dc.description.abstractIncreasingly, evidence supports the function of the helix-loop-helix protein Id-1 (inhibitor of differentiation/DNA binding-1) as an oncogene. Over-expression of Id-1 is not only observed in many types of human cancer but its expression levels have been correlated with cancer progression. However, little is known about the molecular mechanisms responsible for the function of Id-1. Recently, we and others reported that Id-1-induced cell proliferation was mediated through a Raf/MEK signalling pathway. In this study, we investigated if ectopic Id-1 expression in nasopharyngeal carcinoma cells had any protective effect on taxol-induced death, which is also regulated through Raf/MEK pathway. Using four stable Id-1 transfectant clones, we found that exogenous Id-1 expression led to phosphorylation of Raf-1 and MEK1/2 kinases, which was associated with resistance to taxol. Treatment of the Id-1 expressing cells with a MEK inhibitor, PD098059, resulted in an increased taxol-induced apoptosis rate in Id-1 transfectants compared with the vector control. In addition, the fact that the taxol-induced apoptosis rate, down-regulation of Bcl-2 and up-regulation of Bax were suppressed by PD098059 treatment in Id-1 expressing cells indicates that the Id-1 induced cellular protection against apoptosis is mediated through Raf/MEK signalling pathways. Our results suggest that Id-1 may be an upstream regulator of the Raf/MEK signalling pathway, which plays an essential role in protection against taxol-induced apoptosis. Our evidence also indicates a novel treatment strategy to increase anticancer drug-induced apoptosis through inactivation of the Id-1 protein. © Oxford University Press 2004; all rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_US
dc.relation.ispartofCarcinogenesisen_US
dc.subject.meshAntineoplastic Agents, Phytogenic - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshEnzyme Activationen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1en_US
dc.subject.meshMap Kinase Kinase Kinases - Metabolism - Physiologyen_US
dc.subject.meshNasopharyngeal Neoplasms - Pathology - Physiopathologyen_US
dc.subject.meshPaclitaxel - Pharmacologyen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProto-Oncogene Proteins C-Raf - Metabolism - Physiologyen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTranscription Factors - Physiologyen_US
dc.titleId-1-induced Raf/MEK pathway activation is essential for its protective role against taxol-induced apoptosis in nasopharyngeal carcinoma cellsen_US
dc.typeArticleen_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.identifier.authorityTsao, SW=rp00399en_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/carcin/bgh087en_US
dc.identifier.pmid14742319en_US
dc.identifier.scopuseid_2-s2.0-3042781699en_US
dc.identifier.hkuros87583-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042781699&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume25en_US
dc.identifier.issue6en_US
dc.identifier.spage881en_US
dc.identifier.epage887en_US
dc.identifier.isiWOS:000221750400004-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridCheung, HW=7201839469en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridWang, X=7501854829en_US

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