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Article: Id-1 expression promotes cell survival through activation of NF-κB signalling pathway in prostate cancer cells

TitleId-1 expression promotes cell survival through activation of NF-κB signalling pathway in prostate cancer cells
Authors
Issue Date2003
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2003, v. 22 n. 29, p. 4498-4508 How to Cite?
AbstractThe growth-promoting effect of Id-1 (inhibitor of differentiation/DNA binding) has been demonstrated in a number of human cancers. However, the mechanisms responsible for its action are not clear. In this study, we report that in prostate cancer cells, Id-1 promotes cell survival through activation of nuclear factor-κB (NF-κB) signalling pathway. After stable expression of Id-1 protein in LNCaP cells, we found that the Id-1 transfectants showed increased resistance to apoptosis induced by TNFα through inactivation of Bax and caspase 3. In addition, in the LNCaP cells expressing ectopic Id-1 protein, we also observed increased NF-κB transactivation activity and nuclear translocation of the p65 and pS0 proteins, which was accompanied by upregulation of their downstream effectors Bcl-xL and ICAM-1. These results indicate that the Id-1-induced antiapoptotic effect may be via NF-κB signalling transduction pathway in these cells. In addition, inactivation of Id-1 by its antisense oligonucleotide and retroviral construct in DU145 cells resulted in the decrease of nuclear level of p65 and p50 proteins, which was associated with increased sensitivity to TNFα-induced apoptosis. Our results strongly suggest that Id-1 may be one of the upstream regulators of NF-κB and activation of NF-κB signalling pathway may be essential for Id-1 induced cell proliferation through protection against apoptosis. Our findings also suggest a potential therapeutic strategy in which inactivation of Id-1 may lead to sensitization of prostate cancer cells to chemotherapeutic drug-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/149621
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorOuyang, XSen_US
dc.contributor.authorXu, Ken_US
dc.contributor.authorTsao, SWen_US
dc.contributor.authorWong, YCen_US
dc.date.accessioned2012-06-26T05:56:11Z-
dc.date.available2012-06-26T05:56:11Z-
dc.date.issued2003en_US
dc.identifier.citationOncogene, 2003, v. 22 n. 29, p. 4498-4508en_US
dc.identifier.issn0950-9232en_US
dc.identifier.urihttp://hdl.handle.net/10722/149621-
dc.description.abstractThe growth-promoting effect of Id-1 (inhibitor of differentiation/DNA binding) has been demonstrated in a number of human cancers. However, the mechanisms responsible for its action are not clear. In this study, we report that in prostate cancer cells, Id-1 promotes cell survival through activation of nuclear factor-κB (NF-κB) signalling pathway. After stable expression of Id-1 protein in LNCaP cells, we found that the Id-1 transfectants showed increased resistance to apoptosis induced by TNFα through inactivation of Bax and caspase 3. In addition, in the LNCaP cells expressing ectopic Id-1 protein, we also observed increased NF-κB transactivation activity and nuclear translocation of the p65 and pS0 proteins, which was accompanied by upregulation of their downstream effectors Bcl-xL and ICAM-1. These results indicate that the Id-1-induced antiapoptotic effect may be via NF-κB signalling transduction pathway in these cells. In addition, inactivation of Id-1 by its antisense oligonucleotide and retroviral construct in DU145 cells resulted in the decrease of nuclear level of p65 and p50 proteins, which was associated with increased sensitivity to TNFα-induced apoptosis. Our results strongly suggest that Id-1 may be one of the upstream regulators of NF-κB and activation of NF-κB signalling pathway may be essential for Id-1 induced cell proliferation through protection against apoptosis. Our findings also suggest a potential therapeutic strategy in which inactivation of Id-1 may lead to sensitization of prostate cancer cells to chemotherapeutic drug-induced apoptosis.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_US
dc.relation.ispartofOncogeneen_US
dc.subject.meshAdenocarcinoma - Metabolism - Pathologyen_US
dc.subject.meshApoptosis - Drug Effects - Physiologyen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshCell Nucleus - Metabolismen_US
dc.subject.meshCell Survival - Physiologyen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1en_US
dc.subject.meshIntercellular Adhesion Molecule-1 - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshOligonucleotides, Antisense - Pharmacologyen_US
dc.subject.meshPoly(Adp-Ribose) Polymerases - Metabolismen_US
dc.subject.meshProstatic Neoplasms - Metabolism - Pathologyen_US
dc.subject.meshProtein Transporten_US
dc.subject.meshProto-Oncogene Proteins - Metabolismen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Metabolismen_US
dc.subject.meshRepressor Proteinsen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshTranscription Factors - Biosynthesis - Drug Effects - Physiologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.subject.meshTumor Suppressor Protein P53 - Metabolismen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
dc.subject.meshBcl-X Proteinen_US
dc.titleId-1 expression promotes cell survival through activation of NF-κB signalling pathway in prostate cancer 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_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1206693en_US
dc.identifier.pmid12881706-
dc.identifier.scopuseid_2-s2.0-0043170868en_US
dc.identifier.hkuros78635-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0043170868&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue29en_US
dc.identifier.spage4498en_US
dc.identifier.epage4508en_US
dc.identifier.isiWOS:000184054700005-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWang, X=7501854829en_US
dc.identifier.scopusauthoridOuyang, XS=8711278300en_US
dc.identifier.scopusauthoridXu, K=7403282051en_US
dc.identifier.scopusauthoridTsao, SW=7102813116en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US

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