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Article: Up-regulation of TWIST in prostate cancer and its implication as a therapeutic target

TitleUp-regulation of TWIST in prostate cancer and its implication as a therapeutic target
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2005, v. 65 n. 12, p. 5153-5162 How to Cite?
AbstractAndrogen-independent metastatic prostate cancer is the main obstacle in the treatment of this cancer. Unlike a majority of solid cancers, prostate cancer usually shows poor response to chemotherapeutic drugs. In this study, we have shown a potential novel target, TWIST, a highly conserved bHLH transcription factor, in the treatment of prostate cancer. Using malignant and nonmalignant prostate tissues, we found that TWIST expression was highly expressed in the majority (90%) of prostate cancer tissues but only in a small percentage (6.7%) of benign prostate hyperplasia. In addition, the TWIST expression levels were positively correlated with Gleason grading and metastasis, indicating its role in the development and progression of prostate cancer. Furthermore, down-regulation of TWIST through small interfering RNA in androgen-independent prostate cancer cell lines, DU145 and PC3, resulted in increased sensitivity to the anticancer drug taxol-induced cell death which was associated with decreased Bcl/Bax ratio, leading to activation of the apoptosis pathway. More importantly, inactivation of TWIST suppressed migration and invasion abilities of androgen-independent prostate cancer cells, which was correlated with induction of E-cadherin expression as well as morphologic and molecular changes associated with mesenchymal to epithelial transition. These results were further confirmed on the androgen-dependent LNCaP cells ectopically expressing the TWIST protein. Our results have identified TWIST as a critical regulator of prostate cancer cell growth and suggest a potential therapeutic approach to inhibit the growth and metastasis of androgen-independent prostate cancer through inactivation of the TWIST gene. © 2005 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/67338
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwok, WKen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorLee, TWen_HK
dc.contributor.authorLau, TCMen_HK
dc.contributor.authorZhou, Cen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorChua, CWen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorChan, FLen_HK
dc.contributor.authorGlackin, Cen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-06T05:54:13Z-
dc.date.available2010-09-06T05:54:13Z-
dc.date.issued2005en_HK
dc.identifier.citationCancer Research, 2005, v. 65 n. 12, p. 5153-5162en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67338-
dc.description.abstractAndrogen-independent metastatic prostate cancer is the main obstacle in the treatment of this cancer. Unlike a majority of solid cancers, prostate cancer usually shows poor response to chemotherapeutic drugs. In this study, we have shown a potential novel target, TWIST, a highly conserved bHLH transcription factor, in the treatment of prostate cancer. Using malignant and nonmalignant prostate tissues, we found that TWIST expression was highly expressed in the majority (90%) of prostate cancer tissues but only in a small percentage (6.7%) of benign prostate hyperplasia. In addition, the TWIST expression levels were positively correlated with Gleason grading and metastasis, indicating its role in the development and progression of prostate cancer. Furthermore, down-regulation of TWIST through small interfering RNA in androgen-independent prostate cancer cell lines, DU145 and PC3, resulted in increased sensitivity to the anticancer drug taxol-induced cell death which was associated with decreased Bcl/Bax ratio, leading to activation of the apoptosis pathway. More importantly, inactivation of TWIST suppressed migration and invasion abilities of androgen-independent prostate cancer cells, which was correlated with induction of E-cadherin expression as well as morphologic and molecular changes associated with mesenchymal to epithelial transition. These results were further confirmed on the androgen-dependent LNCaP cells ectopically expressing the TWIST protein. Our results have identified TWIST as a critical regulator of prostate cancer cell growth and suggest a potential therapeutic approach to inhibit the growth and metastasis of androgen-independent prostate cancer through inactivation of the TWIST gene. © 2005 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAdenocarcinoma - drug therapy - genetics - metabolism - pathologyen_HK
dc.subject.meshApoptosis - drug effects - physiologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshEpithelial Cells - pathologyen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshGene Silencingen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMesoderm - pathologyen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshNuclear Proteins - biosynthesis - geneticsen_HK
dc.subject.meshPaclitaxel - pharmacologyen_HK
dc.subject.meshProstatic Neoplasms - drug therapy - genetics - metabolism - pathologyen_HK
dc.subject.meshTranscription Factors - biosynthesis - geneticsen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTwist Transcription Factoren_HK
dc.subject.meshUp-Regulationen_HK
dc.titleUp-regulation of TWIST in prostate cancer and its implication as a therapeutic targeten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=65&issue=12&spage=5153&epage=5162&date=2005&atitle=Up-regulation+of+TWIST+in+prostate+cancer+and+its+implication+as+a+therapeutic+targeten_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-04-3785en_HK
dc.identifier.pmid15958559-
dc.identifier.scopuseid_2-s2.0-20444453337en_HK
dc.identifier.hkuros104825en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-20444453337&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume65en_HK
dc.identifier.issue12en_HK
dc.identifier.spage5153en_HK
dc.identifier.epage5162en_HK
dc.identifier.isiWOS:000229734300026-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKwok, WK=8578541800en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridLee, TW=8578540600en_HK
dc.identifier.scopusauthoridLau, TCM=17341008600en_HK
dc.identifier.scopusauthoridZhou, C=8643084400en_HK
dc.identifier.scopusauthoridZhang, X=8299216200en_HK
dc.identifier.scopusauthoridChua, CW=9437494600en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridChan, FL=7202586505en_HK
dc.identifier.scopusauthoridGlackin, C=6602704555en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK

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