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Article: Id-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R)
Title | Id-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R) |
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Authors | |
Issue Date | 2004 |
Publisher | Oxford 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/67845 |
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.074 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ling, MT | en_HK |
dc.contributor.author | Wang, X | en_HK |
dc.contributor.author | Lee, DT | en_HK |
dc.contributor.author | Tam, PC | en_HK |
dc.contributor.author | Tsao, SW | en_HK |
dc.contributor.author | Wong, YC | en_HK |
dc.date.accessioned | 2010-09-06T05:58:47Z | - |
dc.date.available | 2010-09-06T05:58:47Z | - |
dc.date.issued | 2004 | en_HK |
dc.identifier.citation | Carcinogenesis, 2004, v. 25 n. 4, p. 517-525 | en_HK |
dc.identifier.issn | 0143-3334 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/67845 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | Oxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/ | en_HK |
dc.relation.ispartof | Carcinogenesis | en_HK |
dc.rights | Carcinogenesis. Copyright © Oxford University Press. | en_HK |
dc.subject.mesh | Adenocarcinoma - pathology | en_HK |
dc.subject.mesh | Androgens - pharmacology | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Cell Division - drug effects - genetics | en_HK |
dc.subject.mesh | Cell Line, Tumor | en_HK |
dc.subject.mesh | Cell Nucleus - physiology | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | Inhibitor of Differentiation Protein 1 | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Nude | en_HK |
dc.subject.mesh | NF-kappa B - antagonists & inhibitors | en_HK |
dc.subject.mesh | Nitriles - pharmacology | en_HK |
dc.subject.mesh | Promoter Regions, Genetic | en_HK |
dc.subject.mesh | Prostatic Neoplasms - pathology | en_HK |
dc.subject.mesh | Receptor, Epidermal Growth Factor - genetics - physiology | en_HK |
dc.subject.mesh | Repressor Proteins | en_HK |
dc.subject.mesh | Sulfones - pharmacology | en_HK |
dc.subject.mesh | Transcription Factors - genetics | en_HK |
dc.subject.mesh | Transfection | en_HK |
dc.subject.mesh | Transplantation, Heterologous | en_HK |
dc.title | Id-1 expression induces androgen-independent prostate cancer cell growth through activation of epidermal growth factor receptor (EGF-R) | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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.email | Ling, MT:patling@hkucc.hku.hk | en_HK |
dc.identifier.email | Tsao, SW:gswtsao@hkucc.hku.hk | en_HK |
dc.identifier.email | Wong, YC:ycwong@hkucc.hku.hk | en_HK |
dc.identifier.authority | Ling, MT=rp00449 | en_HK |
dc.identifier.authority | Tsao, SW=rp00399 | en_HK |
dc.identifier.authority | Wong, YC=rp00316 | en_HK |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1093/carcin/bgh047 | en_HK |
dc.identifier.pmid | 14688027 | - |
dc.identifier.scopus | eid_2-s2.0-3242758854 | en_HK |
dc.identifier.hkuros | 87578 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-3242758854&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 25 | en_HK |
dc.identifier.issue | 4 | en_HK |
dc.identifier.spage | 517 | en_HK |
dc.identifier.epage | 525 | en_HK |
dc.identifier.isi | WOS:000220485700007 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Ling, MT=7102229780 | en_HK |
dc.identifier.scopusauthorid | Wang, X=7501854829 | en_HK |
dc.identifier.scopusauthorid | Lee, DT=7406666118 | en_HK |
dc.identifier.scopusauthorid | Tam, PC=7202539419 | en_HK |
dc.identifier.scopusauthorid | Tsao, SW=7102813116 | en_HK |
dc.identifier.scopusauthorid | Wong, YC=7403041798 | en_HK |
dc.identifier.issnl | 0143-3334 | - |