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Conference Paper: Identification of a novel function of TWIST, a bHLH protein, in the development of acquired taxol resistance in human cancer cells

TitleIdentification of a novel function of TWIST, a bHLH protein, in the development of acquired taxol resistance in human cancer cells
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. 142 Abstract no. 614 How to Cite?
AbstractTaxol is one of the widely used chemotherapeutic drugs against many types of human cancer. While it is considered as one of the most effective anticancer drugs, treatment failure often occurs due to development of acquired resistance. Therefore, it is important to understand the molecular mechanisms responsible for the development of drug resistance. Although it is generally believed that taxol induces cell death through interfering with microtubules leading to mitotic arrest, recent evidence has suggested that taxol-induced cell death also occurs through pathways independent of either microtubule or mitotic arrest. In this study, we report the identification of a novel role for TWIST, a basic helix-loop-helix protein, which plays a central role in cell type determination and differentiation, during generation of acquired resistance to taxol in a nasopharyngeal carcinoma cell line, HNE1-T3, using comparative genome hybridization (CGH) and subsequent RT-PCR and Western blotting. We found that upregulation of TWIST was associated with cellular resistance to taxol but not other drugs with different mechanisms of action. The fact that increased TWIST protein levels were also associated with another microtubule targeting anticancer drug, vincristine, in 4 types of human cancer including nasopharyngeal, bladder, ovarian and prostate, indicates that it may play a central role in the resistance to microtubule disrupting agents. In addition, ectopic expression of TWIST into human cancer cells also led to increased resistance to both taxol and vincristine. Our results indicate a novel mechanism, which leads to resistance to microtubule disrupting anticancer drugs through upregulation of TWIST. Our evidence provides a therapeutic strategy to overcome acquired resistance through inactivation of TWIST expression in human cancer.
Persistent Identifierhttp://hdl.handle.net/10722/95371
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorLee, DTWen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-25T16:00:07Z-
dc.date.available2010-09-25T16:00:07Z-
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. 142 Abstract no. 614en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95371-
dc.description.abstractTaxol is one of the widely used chemotherapeutic drugs against many types of human cancer. While it is considered as one of the most effective anticancer drugs, treatment failure often occurs due to development of acquired resistance. Therefore, it is important to understand the molecular mechanisms responsible for the development of drug resistance. Although it is generally believed that taxol induces cell death through interfering with microtubules leading to mitotic arrest, recent evidence has suggested that taxol-induced cell death also occurs through pathways independent of either microtubule or mitotic arrest. In this study, we report the identification of a novel role for TWIST, a basic helix-loop-helix protein, which plays a central role in cell type determination and differentiation, during generation of acquired resistance to taxol in a nasopharyngeal carcinoma cell line, HNE1-T3, using comparative genome hybridization (CGH) and subsequent RT-PCR and Western blotting. We found that upregulation of TWIST was associated with cellular resistance to taxol but not other drugs with different mechanisms of action. The fact that increased TWIST protein levels were also associated with another microtubule targeting anticancer drug, vincristine, in 4 types of human cancer including nasopharyngeal, bladder, ovarian and prostate, indicates that it may play a central role in the resistance to microtubule disrupting agents. In addition, ectopic expression of TWIST into human cancer cells also led to increased resistance to both taxol and vincristine. Our results indicate a novel mechanism, which leads to resistance to microtubule disrupting anticancer drugs through upregulation of TWIST. Our evidence provides a therapeutic strategy to overcome acquired resistance through inactivation of TWIST expression in human cancer.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleIdentification of a novel function of TWIST, a bHLH protein, in the development of acquired taxol resistance in human cancer cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailGuan, XY: xyguan@hkucc.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLee, DTW: dtwlee@HKUCC.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros95474en_HK
dc.identifier.volume64en_HK
dc.identifier.spage142en_HK

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