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Article: γ-Tocotrienol suppresses prostate cancer cell proliferation and invasion through multiple-signalling pathways

Titleγ-Tocotrienol suppresses prostate cancer cell proliferation and invasion through multiple-signalling pathways
Authors
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 2008, v. 99 n. 11, p. 1832-1841 How to Cite?
AbstractTocotrienol-rich fraction (TRF) has demonstrated antiproliferative effect on prostate cancer (PCa) cells. To elucidate this anticancer property in PCa cells, this study aimed, first, to identify the most potent isomer for eliminating PCa cells; and second, to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of γ-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of pro-caspases and the presence of sub-G1 cell population. Examination of the pro-survival genes revealed that the γ-tocotrienol-induced cell death was associated with suppression of NF-κB, EGF-R and Id family proteins (Id1 and Id3). Meanwhile, γ-tocotrienol treatment also resulted in the induction of JNK-signalling pathway and inhibition of JNK activity by a specific inhibitor (SP600125) was able to partially block the effect of γ-tocotrienol. Interestingly, γ-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and γ-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, a synergistic effect was observed when cells were co-treated with γ-tocotrienol and Docetaxel. Our results suggested that the antiproliferative effect of γ-tocotrienol act through multiple-signalling pathways, and demonstrated for the first time the anti-invasion and chemosensitisation effect of γ-tocotrienol against PCa cells. © 2008 Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/149706
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
Funding AgencyGrant Number
Research Incentive Scheme for Companies (RISC)HKU 7314/01M
HKU7490/03M
7470/04M
Davos Life Science Pte. Ltd.
Funding Information:

This work was supported by Research Incentive Scheme for Companies (RISC) to Davos Life Science Pte. Ltd. and grants to YCW (HKU 7314/01M, HKU7490/03M and 7470/04M). The 3-week (10 February-1 March 2008) work attachment of Miss Yap Wei Ney at YCW's laboratory (Department of Anatomy, HKU) was sponsored by Davos Life Science Pte. Ltd. and YCW's grants.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorYap, WNen_US
dc.contributor.authorChang, PNen_US
dc.contributor.authorHan, HYen_US
dc.contributor.authorLee, DTWen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorYap, YLen_US
dc.date.accessioned2012-06-26T05:57:24Z-
dc.date.available2012-06-26T05:57:24Z-
dc.date.issued2008en_US
dc.identifier.citationBritish Journal Of Cancer, 2008, v. 99 n. 11, p. 1832-1841en_US
dc.identifier.issn0007-0920en_US
dc.identifier.urihttp://hdl.handle.net/10722/149706-
dc.description.abstractTocotrienol-rich fraction (TRF) has demonstrated antiproliferative effect on prostate cancer (PCa) cells. To elucidate this anticancer property in PCa cells, this study aimed, first, to identify the most potent isomer for eliminating PCa cells; and second, to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of γ-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of pro-caspases and the presence of sub-G1 cell population. Examination of the pro-survival genes revealed that the γ-tocotrienol-induced cell death was associated with suppression of NF-κB, EGF-R and Id family proteins (Id1 and Id3). Meanwhile, γ-tocotrienol treatment also resulted in the induction of JNK-signalling pathway and inhibition of JNK activity by a specific inhibitor (SP600125) was able to partially block the effect of γ-tocotrienol. Interestingly, γ-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and γ-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, a synergistic effect was observed when cells were co-treated with γ-tocotrienol and Docetaxel. Our results suggested that the antiproliferative effect of γ-tocotrienol act through multiple-signalling pathways, and demonstrated for the first time the anti-invasion and chemosensitisation effect of γ-tocotrienol against PCa cells. © 2008 Cancer Research.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_US
dc.relation.ispartofBritish Journal of Canceren_US
dc.subject.meshAntineoplastic Agents - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movement - Drug Effectsen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshFlow Cytometryen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshProstatic Neoplasms - Drug Therapyen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshVitamin E - Analogs & Derivatives - Pharmacologyen_US
dc.titleγ-Tocotrienol suppresses prostate cancer cell proliferation and invasion through multiple-signalling pathwaysen_US
dc.typeArticleen_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjc.6604763en_US
dc.identifier.pmid19002171-
dc.identifier.scopuseid_2-s2.0-56749182084en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-56749182084&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume99en_US
dc.identifier.issue11en_US
dc.identifier.spage1832en_US
dc.identifier.epage1841en_US
dc.identifier.isiWOS:000261214000011-
dc.publisher.placeUnited Kingdomen_US
dc.relation.projectThe role of <I>Id-1</I> gene in prostate carcinogenesis and its relationship to invasiveness of prostate cancer-
dc.identifier.scopusauthoridYap, WN=25637949100en_US
dc.identifier.scopusauthoridChang, PN=27267561700en_US
dc.identifier.scopusauthoridHan, HY=24477301600en_US
dc.identifier.scopusauthoridLee, DTW=7406666118en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridYap, YL=7005551975en_US
dc.identifier.citeulike3505954-

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