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Conference Paper: Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization

TitleInactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research
Citation
AACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 529 Abstract no. 2252 How to Cite?
AbstractResistance to anticancer drugs is the major problem in the treatment of many advanced cancers including androgen-independent prostate cancer. Recently, increased expression of Id-1, a helix-loop-helix protein, is reported in several types of advanced cancers. It is suggested that high expression of Id-1 in cancer cells may provide an advantage for survival and inactivation of Id-1 may be able to increase cancer cells’ susceptibility to apoptosis. To test this hypothesis, in this study, using RNA interfering technology, we inactivated the Id-1 gene in two androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated if downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. Using colony forming and MTT assays, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells after taxol treatment. In addition, the si-Id-1 induced sensitization to taxol was associated with activation of apoptosis pathway demonstrated by increased apoptotic index, DNA laddering, sub-G1 phase of the cell cycle, as well as cleaved-PARP and Caspase 3. Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of chemotherapeutic drug-induced apoptosis in androgen- independent prostate cancer cells. Acknowledgements: This work was supported by RGC grants to X. H. Wang (HKU7478/03M) and Y. C. Wong (HKU 7314/01M and HKU7490/03M).
Persistent Identifierhttp://hdl.handle.net/10722/95180
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-25T15:54:09Z-
dc.date.available2010-09-25T15:54:09Z-
dc.date.issued2005en_HK
dc.identifier.citationAACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 529 Abstract no. 2252en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95180-
dc.description.abstractResistance to anticancer drugs is the major problem in the treatment of many advanced cancers including androgen-independent prostate cancer. Recently, increased expression of Id-1, a helix-loop-helix protein, is reported in several types of advanced cancers. It is suggested that high expression of Id-1 in cancer cells may provide an advantage for survival and inactivation of Id-1 may be able to increase cancer cells’ susceptibility to apoptosis. To test this hypothesis, in this study, using RNA interfering technology, we inactivated the Id-1 gene in two androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated if downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. Using colony forming and MTT assays, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells after taxol treatment. In addition, the si-Id-1 induced sensitization to taxol was associated with activation of apoptosis pathway demonstrated by increased apoptotic index, DNA laddering, sub-G1 phase of the cell cycle, as well as cleaved-PARP and Caspase 3. Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of chemotherapeutic drug-induced apoptosis in androgen- independent prostate cancer cells. Acknowledgements: This work was supported by RGC grants to X. H. Wang (HKU7478/03M) and Y. C. Wong (HKU 7314/01M and HKU7490/03M).-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleInactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitizationen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailZhang, X: xmzhang@hkusua.hku.hken_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros97986en_HK
dc.identifier.volume65en_HK
dc.identifier.spage529en_HK

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