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Conference Paper: Inactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugs

TitleInactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugs
Authors
Issue Date2008
Citation
Advances In Experimental Medicine And Biology, 2008, v. 617, p. 565-572 How to Cite?
AbstractResistance 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 Identifierhttp://hdl.handle.net/10722/152056
ISSN
2015 Impact Factor: 1.953
2015 SCImago Journal Rankings: 0.887
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, YCen_US
dc.contributor.authorZhang, XMen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorWang, XHen_US
dc.date.accessioned2012-06-26T06:33:49Z-
dc.date.available2012-06-26T06:33:49Z-
dc.date.issued2008en_US
dc.identifier.citationAdvances In Experimental Medicine And Biology, 2008, v. 617, p. 565-572en_US
dc.identifier.issn0065-2598en_US
dc.identifier.urihttp://hdl.handle.net/10722/152056-
dc.description.abstractResistance 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.languageengen_US
dc.relation.ispartofAdvances in Experimental Medicine and Biologyen_US
dc.subject.meshAntineoplastic Agents, Phytogenic - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshColony-Forming Units Assayen_US
dc.subject.meshDrug Resistance, Neoplasmen_US
dc.subject.meshEnzyme Activation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1 - Antagonists & Inhibitors - Genetics - Metabolismen_US
dc.subject.meshJnk Mitogen-Activated Protein Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasms, Hormone-Dependent - Drug Therapy - Metabolism - Pathologyen_US
dc.subject.meshPaclitaxel - Pharmacologyen_US
dc.subject.meshProstatic Neoplasms - Drug Therapy - Pathologyen_US
dc.subject.meshRna, Small Interfering - Pharmacologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleInactivation of ID-1 gene induces sensitivity of prostate cancer cells to chemotherapeutic drugsen_US
dc.typeConference_Paperen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/978-0-387-69080-3_58en_US
dc.identifier.pmid18497083-
dc.identifier.scopuseid_2-s2.0-46749150093en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-46749150093&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume617en_US
dc.identifier.spage565en_US
dc.identifier.epage572en_US
dc.identifier.isiWOS:000253701800058-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridZhang, XM=8299216200en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWang, XH=7501854829en_US

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