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Conference Paper: Upregulation of TWIST in prostate cancer and its implication as a therapeutic target

TitleUpregulation of TWIST in prostate cancer and its implication as a therapeutic target
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research
Citation
AACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 1312 Abstract no. 5574 How to Cite?
AbstractAndrogen independent and metastatic prostate cancer is the main obstacle in the treatment of this cancer. Unlike majority of solid cancers, prostate cancer usually shows poor response to chemotherapeutic drugs. In this study, we have demonstrated a potential novel target, TWIST, a highly conserved bHLH protein, in the treatment of prostate cancer. Using malignant and non-malignant prostate tissues, we found that TWIST was highly expressed in majority (90%) of prostate cancer tissues but only in small percentage (6.7%) of Benign Prostate Hyperplasia (BPH). In addition, the TWIST expression levels were positively correlated with Gleason grading, indicating its role in the development and progression of prostate cancer. Furthermore, downregulation of TWIST through small RNA interference (RNAi) in androgen independent prostate cancer cells 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 metastatic ability of androgen independent prostate cancer cells which was correlated with morphological and molecular changes associated with mesenchymal to epithelial transition (MET). In contrast, ectopic expression of TWIST in androgen dependent prostate cancer cells resulted in suppression of taxol-induced apoptosis and reversed the MET phenotype. Our results identified TWIST as a critical regulator of androgen independent prostate cancer growth and suggested a potential therapeutic approach to inhibit the growth and metastasis of androgen independent prostate cancer through targeting the TWIST gene.
Persistent Identifierhttp://hdl.handle.net/10722/95137
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorKwok, WKen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorWang, Xen_HK
dc.date.accessioned2010-09-25T15:52:48Z-
dc.date.available2010-09-25T15:52:48Z-
dc.date.issued2005en_HK
dc.identifier.citationAACR 96th Annual Meeting, Anaheim CA, 16–20 April 2005. In Cancer Research, 2005, v. 65 n. 9S, p. 1312 Abstract no. 5574en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/95137-
dc.description.abstractAndrogen independent and metastatic prostate cancer is the main obstacle in the treatment of this cancer. Unlike majority of solid cancers, prostate cancer usually shows poor response to chemotherapeutic drugs. In this study, we have demonstrated a potential novel target, TWIST, a highly conserved bHLH protein, in the treatment of prostate cancer. Using malignant and non-malignant prostate tissues, we found that TWIST was highly expressed in majority (90%) of prostate cancer tissues but only in small percentage (6.7%) of Benign Prostate Hyperplasia (BPH). In addition, the TWIST expression levels were positively correlated with Gleason grading, indicating its role in the development and progression of prostate cancer. Furthermore, downregulation of TWIST through small RNA interference (RNAi) in androgen independent prostate cancer cells 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 metastatic ability of androgen independent prostate cancer cells which was correlated with morphological and molecular changes associated with mesenchymal to epithelial transition (MET). In contrast, ectopic expression of TWIST in androgen dependent prostate cancer cells resulted in suppression of taxol-induced apoptosis and reversed the MET phenotype. Our results identified TWIST as a critical regulator of androgen independent prostate cancer growth and suggested a potential therapeutic approach to inhibit the growth and metastasis of androgen independent prostate cancer through targeting the TWIST gene.-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Researchen_HK
dc.titleUpregulation of TWIST in prostate cancer and its implication as a therapeutic targeten_HK
dc.typeConference_Paperen_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros98016en_HK
dc.identifier.volume65en_HK
dc.identifier.spage1312en_HK

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