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

TitleId-1-induced Raf/MEK pathway activation is essential for its protective role against apoptosis in nasopharyngeal carcinoma cells
Authors
Issue Date2004
PublisherAmerican Association for Cancer Research
Citation
AACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 20 Abstract no. 87 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. Overexpression 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 (NPC) cells had any protective effect on taxol-induced apoptosis, 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 to the vector control. In addition, the fact that the taxol-induced apoptosis rate, downregulation of Bcl-2 and upregulation 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 these 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.
Persistent Identifierhttp://hdl.handle.net/10722/94934
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-25T15:46:28Z-
dc.date.available2010-09-25T15:46:28Z-
dc.date.issued2004en_HK
dc.identifier.citationAACR 95th Annual Meeting, Orlando FL, 27–31 March 2004. In Cancer Research, 2004, v. 64 n. 7S, p. 20 Abstract no. 87en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/94934-
dc.description.abstractIncreasingly, evidence supports the function of the helix-loop-helix protein Id-1 (inhibitor of differentiation/DNA binding-1) as an oncogene. Overexpression 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 (NPC) cells had any protective effect on taxol-induced apoptosis, 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 to the vector control. In addition, the fact that the taxol-induced apoptosis rate, downregulation of Bcl-2 and upregulation 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 these 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.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleId-1-induced Raf/MEK pathway activation is essential for its protective role against apoptosis in nasopharyngeal carcinoma cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros95440en_HK
dc.identifier.volume64en_HK
dc.identifier.spage20en_HK

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