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Article: 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
KeywordsCancer
Resistance
Taxol
Twist
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2004, v. 23 n. 2, p. 474-482 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 four 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 that 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/10722/67550
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorLee, DTen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:56:08Z-
dc.date.available2010-09-06T05:56:08Z-
dc.date.issued2004en_HK
dc.identifier.citationOncogene, 2004, v. 23 n. 2, p. 474-482en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67550-
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 four 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 that 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.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectCanceren_HK
dc.subjectResistanceen_HK
dc.subjectTaxolen_HK
dc.subjectTwisten_HK
dc.subject.meshDrug Resistance, Neoplasmen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHelix-Loop-Helix Motifsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitory Concentration 50en_HK
dc.subject.meshMaleen_HK
dc.subject.meshNasopharyngeal Neoplasms - drug therapy - metabolism - pathologyen_HK
dc.subject.meshNuclear Proteins - chemistry - genetics - metabolismen_HK
dc.subject.meshOvarian Neoplasms - geneticsen_HK
dc.subject.meshPaclitaxel - pharmacologyen_HK
dc.subject.meshProstatic Neoplasms - geneticsen_HK
dc.subject.meshTranscription Factorsen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTwist Transcription Factoren_HK
dc.subject.meshUrinary Bladder Neoplasms - geneticsen_HK
dc.subject.meshVincristine - pharmacologyen_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.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=23&spage=474&epage=482&date=2004&atitle=Identification+of+a+novel+function+of+TWIST,+a+bHLH+protein,+in+the+development+of+acquired+taxol+resistance+in+human+cancer+cellsen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@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, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/sj.onc.1207128en_HK
dc.identifier.pmid14724576-
dc.identifier.scopuseid_2-s2.0-0842286741en_HK
dc.identifier.hkuros87581en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842286741&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue2en_HK
dc.identifier.spage474en_HK
dc.identifier.epage482en_HK
dc.identifier.isiWOS:000188098300018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridCheung, HW=7201839381en_HK
dc.identifier.scopusauthoridLee, DT=7406666118en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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