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

TitleId-1 expression induces androgen independent prostate cancer cell growth through activation of epithelial growth factor receptor (EGF-R)
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. 1032 Abstract no. 4472 How to Cite?
AbstractThe failure of prostate cancer treatment is largely due to the development of androgen independence, since androgen depletion therapy remains the front-line option for this cancer. Previously, we reported that over-expression of the helix-loop-helix (HLH) 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 whether 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 upregulation of EGF-R (epithelial 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. Our results suggest that upregulation 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 and PSA expression. Inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of androgen independent prostate cancer cell growth. [This work was supported by RGC grants to YCW (HKU7186/99M, HKU7314/01M and HKU7490/03M) and Area of Excellence Scheme (Project No. AoE/P-10/01)].
Persistent Identifierhttp://hdl.handle.net/10722/95540
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorTsao, GSWen_HK
dc.date.accessioned2010-09-25T16:05:29Z-
dc.date.available2010-09-25T16:05:29Z-
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. 1032 Abstract no. 4472en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95540-
dc.description.abstractThe failure of prostate cancer treatment is largely due to the development of androgen independence, since androgen depletion therapy remains the front-line option for this cancer. Previously, we reported that over-expression of the helix-loop-helix (HLH) 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 whether 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 upregulation of EGF-R (epithelial 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. Our results suggest that upregulation 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 and PSA expression. Inactivation of Id-1 may provide a potential therapeutic strategy leading to inhibition of androgen independent prostate cancer cell growth. [This work was supported by RGC grants to YCW (HKU7186/99M, HKU7314/01M and HKU7490/03M) and Area of Excellence Scheme (Project No. AoE/P-10/01)].-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleId-1 expression induces androgen independent prostate cancer cell growth through activation of epithelial growth factor receptor (EGF-R)en_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.hkuros95477en_HK
dc.identifier.volume64en_HK
dc.identifier.spage1032en_HK

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