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Article: Id-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R)

TitleId-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R)
Authors
Issue Date2004
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2004, v. 25 n. 4, p. 517-525 How to Cite?
AbstractThe failure of prostate cancer treatment is largely due to the development of androgen independence, since the androgen depletion therapy remains the front-line option for this cancer. Previously, we reported that over-expression of the helix-loop-helix protein Id-1 was associated with progression of prostate cancer and ectopic expression of Id-1 induced serum-independent proliferation in prostate cancer cells. In the present study, we investigated if exogenous Id-1 expression in the androgen sensitive LNCaP cells had any effect on androgen-dependent cell growth and studied the molecular mechanisms involved. Using stable Id-1 transfectants, we found that expression of Id-1 was able to reduce androgen-stimulated growth and S phase fraction of the cell cycle in LNCaP cells, indicating that Id-1 may be involved in the development of androgen independence in these cells. The Id-1-induced androgen-independent prostate cancer cell growth was correlated with up-regulation of EGF-R (epidermal growth factor-receptor) and PSA (prostate specific antigen) expression, as confirmed by western blotting analysis and luciferase assays. In contrast, down-regulation of Id-1 in androgen-independent DU145 cells by its antisense oligonucleotides resulted in suppression of EGF-R expression at both transcriptional and protein levels. In addition, the results from immunohistochemistry study showed that Id-1 expression was significantly elevated in hormone refractory prostate cancer tissues when compared with the hormone-dependent tumours. Our results suggest that up-regulation of Id-1 in prostate cancer cells may be one of the mechanisms responsible for developing androgen independence and this process may be regulated through induction of EGF-R expression. Inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of androgen-independent prostate cancer cell growth. © Oxford University Press 2004; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67845
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLee, DTen_HK
dc.contributor.authorTam, PCen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:58:47Z-
dc.date.available2010-09-06T05:58:47Z-
dc.date.issued2004en_HK
dc.identifier.citationCarcinogenesis, 2004, v. 25 n. 4, p. 517-525en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67845-
dc.description.abstractThe failure of prostate cancer treatment is largely due to the development of androgen independence, since the androgen depletion therapy remains the front-line option for this cancer. Previously, we reported that over-expression of the helix-loop-helix protein Id-1 was associated with progression of prostate cancer and ectopic expression of Id-1 induced serum-independent proliferation in prostate cancer cells. In the present study, we investigated if exogenous Id-1 expression in the androgen sensitive LNCaP cells had any effect on androgen-dependent cell growth and studied the molecular mechanisms involved. Using stable Id-1 transfectants, we found that expression of Id-1 was able to reduce androgen-stimulated growth and S phase fraction of the cell cycle in LNCaP cells, indicating that Id-1 may be involved in the development of androgen independence in these cells. The Id-1-induced androgen-independent prostate cancer cell growth was correlated with up-regulation of EGF-R (epidermal growth factor-receptor) and PSA (prostate specific antigen) expression, as confirmed by western blotting analysis and luciferase assays. In contrast, down-regulation of Id-1 in androgen-independent DU145 cells by its antisense oligonucleotides resulted in suppression of EGF-R expression at both transcriptional and protein levels. In addition, the results from immunohistochemistry study showed that Id-1 expression was significantly elevated in hormone refractory prostate cancer tissues when compared with the hormone-dependent tumours. Our results suggest that up-regulation of Id-1 in prostate cancer cells may be one of the mechanisms responsible for developing androgen independence and this process may be regulated through induction of EGF-R expression. Inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of androgen-independent prostate cancer cell growth. © Oxford University Press 2004; all rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshAdenocarcinoma - pathologyen_HK
dc.subject.meshAndrogens - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Division - drug effects - geneticsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Nucleus - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInhibitor of Differentiation Protein 1en_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNF-kappa B - antagonists & inhibitorsen_HK
dc.subject.meshNitriles - pharmacologyen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshProstatic Neoplasms - pathologyen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - genetics - physiologyen_HK
dc.subject.meshRepressor Proteinsen_HK
dc.subject.meshSulfones - pharmacologyen_HK
dc.subject.meshTranscription Factors - geneticsen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTransplantation, Heterologousen_HK
dc.titleId-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R)en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=25 No 4&spage=517&epage=525&date=2004&atitle=Id-1+expression+induces+androgen-independent+prostate+cancer+cell+growth+through+activation+of+epidermal+growth+factor+receptor+(EGF-R)en_HK
dc.identifier.emailLing, MT:patling@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.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/carcin/bgh047en_HK
dc.identifier.pmid14688027-
dc.identifier.scopuseid_2-s2.0-3242758854en_HK
dc.identifier.hkuros87578en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3242758854&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume25en_HK
dc.identifier.issue4en_HK
dc.identifier.spage517en_HK
dc.identifier.epage525en_HK
dc.identifier.isiWOS:000220485700007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLee, DT=7406666118en_HK
dc.identifier.scopusauthoridTam, PC=7202539419en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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