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Conference Paper: Caveolin-1, a novel Id1 binding partner, and its role on Id1-induced behavioral change in prostate cancer cells

TitleCaveolin-1, a novel Id1 binding partner, and its role on Id1-induced behavioral change in prostate cancer cells
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research.
Citation
The 99th Annual Meeting of the American Association for Cancer Research (AACR 2008), San Diego, CA., 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, p. 4546 How to Cite?
AbstractId-1 (Inhibitor of Differentiation/DNA binding-1) is reported to promote cell proliferation, invasion and survival in many types of human cancer cells through multiple signaling pathways. In this study, we identified a novel Id-1 interacting protein, caveolin-1 (Cav-1), a cell membrane protein and a positive regulator of cell survival and metastasis in prostate cancer. Using immunoprecipitation method, we found that the helix-loop-helix domain of the Id-1 protein was essential for the physical interaction between Id-1 and Cav-1. We also demonstrated in prostate cancer cells that the physical interaction between Id-1 and Cav-1 played a key role in the Id-1-induced epithelial-mesenchymal transition and cell migration as well as resistance to taxol-induced apoptosis. Our results also revealed that the Id-1-induced Akt activation through promoting the binding activity between Cav-1 and PP2A phosphatase was responsible for the synergistic effect between these two proteins. Our study demonstrates a novel Id-1 binding partner and suggests a molecular mechanism that mediates the function of Id-1 in promoting prostate cancer cell invasion and survival through activation of the Akt pathway [(HKU7478/03M) to XHW and YCW (HKU7490.03M, 7470/04M, NSFC/RGC N_HKU738/03, HKU Foundation Seed Fund, 03)].
Persistent Identifierhttp://hdl.handle.net/10722/95600
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-25T16:07:21Z-
dc.date.available2010-09-25T16:07:21Z-
dc.date.issued2008en_HK
dc.identifier.citationThe 99th Annual Meeting of the American Association for Cancer Research (AACR 2008), San Diego, CA., 12-16 April 2008. In Cancer Research, 2008, v. 68 n. 9S, p. 4546en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95600-
dc.description.abstractId-1 (Inhibitor of Differentiation/DNA binding-1) is reported to promote cell proliferation, invasion and survival in many types of human cancer cells through multiple signaling pathways. In this study, we identified a novel Id-1 interacting protein, caveolin-1 (Cav-1), a cell membrane protein and a positive regulator of cell survival and metastasis in prostate cancer. Using immunoprecipitation method, we found that the helix-loop-helix domain of the Id-1 protein was essential for the physical interaction between Id-1 and Cav-1. We also demonstrated in prostate cancer cells that the physical interaction between Id-1 and Cav-1 played a key role in the Id-1-induced epithelial-mesenchymal transition and cell migration as well as resistance to taxol-induced apoptosis. Our results also revealed that the Id-1-induced Akt activation through promoting the binding activity between Cav-1 and PP2A phosphatase was responsible for the synergistic effect between these two proteins. Our study demonstrates a novel Id-1 binding partner and suggests a molecular mechanism that mediates the function of Id-1 in promoting prostate cancer cell invasion and survival through activation of the Akt pathway [(HKU7478/03M) to XHW and YCW (HKU7490.03M, 7470/04M, NSFC/RGC N_HKU738/03, HKU Foundation Seed Fund, 03)].-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.-
dc.relation.ispartofCancer Researchen_HK
dc.titleCaveolin-1, a novel Id1 binding partner, and its role on Id1-induced behavioral change in prostate cancer cellsen_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.authorityWong, YC=rp00316en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.hkuros147365en_HK
dc.identifier.volume68-
dc.identifier.issue9S-
dc.identifier.spage4546-
dc.identifier.epage4546-

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