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- Publisher Website: 10.1007/978-0-387-69080-3_58
- Scopus: eid_2-s2.0-46749150093
- PMID: 18497083
- WOS: WOS:000253701800058
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Conference Paper: Inactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugs
Title | Inactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugs |
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Authors | |
Issue Date | 2008 |
Citation | Advances In Experimental Medicine And Biology, 2008, v. 617, p. 565-572 How to Cite? |
Abstract | Resistance to anticancer drags is one of the major reasons of treatment failure for androgen-independent prostate cancer (PC). Increase in expression of Id-1 has been reported in several types of advanced cancer including PC. It has been suggested that overexpression of Id-1 may provide an advantage for cancer cell survival and thus inactivation of Id-1 may be able to increase the susceptibility of cancer cells to apoptosis. In this study, using small RNA interfering (siRNA) technology, we inactivated the Id-1 gene in two androgen-independent PC cell lines, DU145 and PC3, and investigated whether down-regulation of Id-1 could lead to increased sensitivity of these PC cells to a commonly used anticancer drug, taxol (Tx). Our results showed that inactivation of Id-1 by sild-1 resulted in decrease in both colony forming ability and cell viability in prostate cancer cells after Tx treatment. Furthermore, the sild-1 induced sensitization to Tx was associated with activation of apoptotic pathway. In addition, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for Tx-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the sild-1-induced sensitivity to Tx. These results indicate that increased Id-1 expression in PC cells may play a protective role against apoptosis, and down-regulation of Id-1 may be a potential target to increase sensitivity of Tx-induced apoptosis in PC cells. © 2008 Springer Science+Business Media, LLC. |
Persistent Identifier | http://hdl.handle.net/10722/152056 |
ISSN | 2021 Impact Factor: 3.650 2023 SCImago Journal Rankings: 0.244 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wong, YC | en_US |
dc.contributor.author | Zhang, XM | en_US |
dc.contributor.author | Ling, MT | en_US |
dc.contributor.author | Wang, XH | en_US |
dc.date.accessioned | 2012-06-26T06:33:49Z | - |
dc.date.available | 2012-06-26T06:33:49Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | Advances In Experimental Medicine And Biology, 2008, v. 617, p. 565-572 | en_US |
dc.identifier.issn | 0065-2598 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/152056 | - |
dc.description.abstract | Resistance to anticancer drags is one of the major reasons of treatment failure for androgen-independent prostate cancer (PC). Increase in expression of Id-1 has been reported in several types of advanced cancer including PC. It has been suggested that overexpression of Id-1 may provide an advantage for cancer cell survival and thus inactivation of Id-1 may be able to increase the susceptibility of cancer cells to apoptosis. In this study, using small RNA interfering (siRNA) technology, we inactivated the Id-1 gene in two androgen-independent PC cell lines, DU145 and PC3, and investigated whether down-regulation of Id-1 could lead to increased sensitivity of these PC cells to a commonly used anticancer drug, taxol (Tx). Our results showed that inactivation of Id-1 by sild-1 resulted in decrease in both colony forming ability and cell viability in prostate cancer cells after Tx treatment. Furthermore, the sild-1 induced sensitization to Tx was associated with activation of apoptotic pathway. In addition, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for Tx-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the sild-1-induced sensitivity to Tx. These results indicate that increased Id-1 expression in PC cells may play a protective role against apoptosis, and down-regulation of Id-1 may be a potential target to increase sensitivity of Tx-induced apoptosis in PC cells. © 2008 Springer Science+Business Media, LLC. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Advances in Experimental Medicine and Biology | en_US |
dc.subject.mesh | Antineoplastic Agents, Phytogenic - Pharmacology | en_US |
dc.subject.mesh | Apoptosis - Drug Effects | en_US |
dc.subject.mesh | Colony-Forming Units Assay | en_US |
dc.subject.mesh | Drug Resistance, Neoplasm | en_US |
dc.subject.mesh | Enzyme Activation - Drug Effects | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Inhibitor Of Differentiation Protein 1 - Antagonists & Inhibitors - Genetics - Metabolism | en_US |
dc.subject.mesh | Jnk Mitogen-Activated Protein Kinases - Antagonists & Inhibitors - Metabolism | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Neoplasms, Hormone-Dependent - Drug Therapy - Metabolism - Pathology | en_US |
dc.subject.mesh | Paclitaxel - Pharmacology | en_US |
dc.subject.mesh | Prostatic Neoplasms - Drug Therapy - Pathology | en_US |
dc.subject.mesh | Rna, Small Interfering - Pharmacology | en_US |
dc.subject.mesh | Tumor Cells, Cultured | en_US |
dc.title | Inactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugs | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Wong, YC:ycwong@hkucc.hku.hk | en_US |
dc.identifier.email | Ling, MT:patling@hkucc.hku.hk | en_US |
dc.identifier.authority | Wong, YC=rp00316 | en_US |
dc.identifier.authority | Ling, MT=rp00449 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1007/978-0-387-69080-3_58 | en_US |
dc.identifier.pmid | 18497083 | - |
dc.identifier.scopus | eid_2-s2.0-46749150093 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-46749150093&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 617 | en_US |
dc.identifier.spage | 565 | en_US |
dc.identifier.epage | 572 | en_US |
dc.identifier.isi | WOS:000253701800058 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Wong, YC=7403041798 | en_US |
dc.identifier.scopusauthorid | Zhang, XM=8299216200 | en_US |
dc.identifier.scopusauthorid | Ling, MT=7102229780 | en_US |
dc.identifier.scopusauthorid | Wang, XH=7501854829 | en_US |
dc.customcontrol.immutable | sml 161206 - amend | - |
dc.identifier.issnl | 0065-2598 | - |