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Article: Activation of MAPK signaling pathway is essential for Id-1 induced serum independent prostate cancer cell growth

TitleActivation of MAPK signaling pathway is essential for Id-1 induced serum independent prostate cancer cell growth
Authors
KeywordsCell growth
Id-1
MAPK
Prostate cancer
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2002, v. 21 n. 55, p. 8498-8505 How to Cite?
AbstractThe helix-loop-helix protein Id-1 has been suggested to play a positive role in cell proliferation and tumorigenesis of many types of human cancers. However, little is known about the molecular mechanism involved in the function of Id-1. In this study, using four stable Id-1 transfectant clones, we investigated the involvement of MAPK signaling pathway in the Id-1 induced serum independent prostate cancer cell growth. Our results demonstrated that both transient and stable ectopic Id-1 expression in prostate cancer LNCaP cells led to activation of the Raf/MEK1/2 signaling pathway. In addition, inhibition of MEK1/2 phosphorylation by one of its inhibitors, PD098059, resulted in the decreased cell cycle S phase fraction and cell growth rate, suggesting that activation of MAPK signaling pathway is essential for Id-1 induced prostate cancer cell proliferation. Furthermore, treatment with antisense oligonucleotide complementary to Id-1 mRNA in PC-3 and DU145 cells resulted in a decreased Id-1 expression which was accompanied by decreased Egr-1 protein. Our results suggest for the first time that the function of Id-1 is associated with MAPK signaling pathway activation and indicate a possible novel mechanism in which Id-1 regulates prostate cancer cell growth and tumorigenesis.
Persistent Identifierhttp://hdl.handle.net/10722/148305
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorOuyang, XSen_HK
dc.contributor.authorLee, TKWen_HK
dc.contributor.authorFan, TYen_HK
dc.contributor.authorXu, Ken_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2012-05-29T06:12:07Z-
dc.date.available2012-05-29T06:12:07Z-
dc.date.issued2002en_HK
dc.identifier.citationOncogene, 2002, v. 21 n. 55, p. 8498-8505en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148305-
dc.description.abstractThe helix-loop-helix protein Id-1 has been suggested to play a positive role in cell proliferation and tumorigenesis of many types of human cancers. However, little is known about the molecular mechanism involved in the function of Id-1. In this study, using four stable Id-1 transfectant clones, we investigated the involvement of MAPK signaling pathway in the Id-1 induced serum independent prostate cancer cell growth. Our results demonstrated that both transient and stable ectopic Id-1 expression in prostate cancer LNCaP cells led to activation of the Raf/MEK1/2 signaling pathway. In addition, inhibition of MEK1/2 phosphorylation by one of its inhibitors, PD098059, resulted in the decreased cell cycle S phase fraction and cell growth rate, suggesting that activation of MAPK signaling pathway is essential for Id-1 induced prostate cancer cell proliferation. Furthermore, treatment with antisense oligonucleotide complementary to Id-1 mRNA in PC-3 and DU145 cells resulted in a decreased Id-1 expression which was accompanied by decreased Egr-1 protein. Our results suggest for the first time that the function of Id-1 is associated with MAPK signaling pathway activation and indicate a possible novel mechanism in which Id-1 regulates prostate cancer cell growth and tumorigenesis.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectCell growthen_HK
dc.subjectId-1en_HK
dc.subjectMAPKen_HK
dc.subjectProstate canceren_HK
dc.subject.meshCell Divisionen_US
dc.subject.meshDna-Binding Proteins - Geneticsen_US
dc.subject.meshEarly Growth Response Protein 1en_US
dc.subject.meshHelix-Loop-Helix Motifsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmediate-Early Proteinsen_US
dc.subject.meshInhibitor Of Differentiation Protein 1en_US
dc.subject.meshMap Kinase Signaling System - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshProstatic Neoplasms - Pathologyen_US
dc.subject.meshRecombinant Proteins - Metabolismen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshTranscription Factors - Genetics - Physiologyen_US
dc.subject.meshTransfectionen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleActivation of MAPK signaling pathway is essential for Id-1 induced serum independent prostate cancer cell growthen_HK
dc.typeArticleen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailLee, TKW:tkwlee@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityLee, TKW=rp00447en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1206007en_HK
dc.identifier.pmid12466969-
dc.identifier.scopuseid_2-s2.0-0037028212en_HK
dc.identifier.hkuros75836-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037028212&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issue55en_HK
dc.identifier.spage8498en_HK
dc.identifier.epage8505en_HK
dc.identifier.isiWOS:000179480100012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridOuyang, XS=8711278300en_HK
dc.identifier.scopusauthoridLee, TKW=7501439435en_HK
dc.identifier.scopusauthoridFan, TY=7202528808en_HK
dc.identifier.scopusauthoridXu, K=7403282051en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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