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Article: Evidence of -tocotrienol as an apoptosis-inducing, invasion-suppressing, and chemotherapy drug-sensitizing agent in human melanoma cells

TitleEvidence of -tocotrienol as an apoptosis-inducing, invasion-suppressing, and chemotherapy drug-sensitizing agent in human melanoma cells
Authors
Issue Date2009
PublisherLawrence Erlbaum Associates, Inc. The Journal's web site is located at http://www.leaonline.com/loi/nc
Citation
Nutrition And Cancer, 2009, v. 61 n. 3, p. 357-366 How to Cite?
AbstractTo date, the most effective cure for metastatic melanoma remains the surgical resection of the primary tumor. Recently, tocotrienol-rich-fraction has shown antiproliferative effect on cancer cells. To elucidate this anticancer property in malignant melanoma, this study aimed, first, to identify the most potent isomer for eliminating melanoma cells and second to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of gamma-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of procaspases and the accumulation of sub-G1 cell population. Examination of the prosurvival genes revealed that the gamma-tocotrienol-induced cell death was associated with suppression of NF-kappaB, EGF-R, and Id family proteins. Meanwhile, gamma-tocotrienol treatment also resulted in induction of JNK signaling pathway, and inhibition of JNK activity by selective inhibitor was able to partially block the effect of gamma-tocotrienol. Interestingly, gamma-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and gamma-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, synergistic effect was observed when cells were cotreated with gamma-tocotrienol and chemotherapy drugs. Together, our results demonstrated for the first time the anti-invasion and chemonsensitization effect of gamma-tocotrienol against human malignant melanoma cells.
Persistent Identifierhttp://hdl.handle.net/10722/149719
ISSN
2015 Impact Factor: 2.241
2015 SCImago Journal Rankings: 0.931
ISI Accession Number ID
Funding AgencyGrant Number
Research Incentive Scheme for Companies (RISC)
Davos Life Science Pte. Ltd7314/01M
HKU7490/03M
7470/04M
Funding Information:

This work was supported by Research Incentive Scheme for Companies (RISC) to Davos Life Science Pte. Ltd. and grants to Y. C. Wong (HKU 7314/01M, HKU7490/03M, and 7470/04M). We thank Yee Lino Tan for assistances on settin up the cell invasion assay. Pick Ngoh Chang and Wei Ney Yap contributed equally to this work.

References

 

DC FieldValueLanguage
dc.contributor.authorChang, PNen_US
dc.contributor.authorYap, WNen_US
dc.contributor.authorWing Lee, DTen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorYap, YLen_US
dc.date.accessioned2012-06-26T05:57:35Z-
dc.date.available2012-06-26T05:57:35Z-
dc.date.issued2009en_US
dc.identifier.citationNutrition And Cancer, 2009, v. 61 n. 3, p. 357-366en_US
dc.identifier.issn0163-5581en_US
dc.identifier.urihttp://hdl.handle.net/10722/149719-
dc.description.abstractTo date, the most effective cure for metastatic melanoma remains the surgical resection of the primary tumor. Recently, tocotrienol-rich-fraction has shown antiproliferative effect on cancer cells. To elucidate this anticancer property in malignant melanoma, this study aimed, first, to identify the most potent isomer for eliminating melanoma cells and second to decipher the molecular pathway responsible for its activity. Results showed that the inhibitory effect of gamma-tocotrienol was most potent, which resulted in induction of apoptosis as evidenced by activation of procaspases and the accumulation of sub-G1 cell population. Examination of the prosurvival genes revealed that the gamma-tocotrienol-induced cell death was associated with suppression of NF-kappaB, EGF-R, and Id family proteins. Meanwhile, gamma-tocotrienol treatment also resulted in induction of JNK signaling pathway, and inhibition of JNK activity by selective inhibitor was able to partially block the effect of gamma-tocotrienol. Interestingly, gamma-tocotrienol treatment led to suppression of mesenchymal markers and the restoration of E-cadherin and gamma-catenin expression, which was associated with suppression of cell invasion capability. Furthermore, synergistic effect was observed when cells were cotreated with gamma-tocotrienol and chemotherapy drugs. Together, our results demonstrated for the first time the anti-invasion and chemonsensitization effect of gamma-tocotrienol against human malignant melanoma cells.en_US
dc.languageengen_US
dc.publisherLawrence Erlbaum Associates, Inc. The Journal's web site is located at http://www.leaonline.com/loi/ncen_US
dc.relation.ispartofNutrition and Canceren_US
dc.subject.meshAntineoplastic Agents - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCadherins - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshDacarbazine - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshJnk Mitogen-Activated Protein Kinases - Physiologyen_US
dc.subject.meshMelanoma - Drug Therapy - Pathologyen_US
dc.subject.meshNeoplasm Invasivenessen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTaxoids - Pharmacologyen_US
dc.subject.meshVitamin E - Analogs & Derivatives - Pharmacologyen_US
dc.titleEvidence of -tocotrienol as an apoptosis-inducing, invasion-suppressing, and chemotherapy drug-sensitizing agent in human melanoma cellsen_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.doi10.1080/01635580802567166en_US
dc.identifier.pmid19373609-
dc.identifier.scopuseid_2-s2.0-67649399439en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649399439&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume61en_US
dc.identifier.issue3en_US
dc.identifier.spage357en_US
dc.identifier.epage366en_US
dc.identifier.isiWOS:000268242000009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChang, PN=27267561700en_US
dc.identifier.scopusauthoridYap, WN=25637949100en_US
dc.identifier.scopusauthoridWing Lee, DT=35276533400en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridYap, YL=7005551975en_US

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