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- Publisher Website: 10.1038/sj.onc.1206370
- Scopus: eid_2-s2.0-0038297516
- PMID: 12687016
- WOS: WOS:000182066900008
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Article: Inhibition of cell transformation by resveratrol and its derivatives: Differential effects and mechanisms involved
Title | Inhibition of cell transformation by resveratrol and its derivatives: Differential effects and mechanisms involved |
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Authors | |
Keywords | Cell transformation Chemoprevention p53 PI-3K/Akt Resveratrol Resveratrol derivatives |
Issue Date | 2003 |
Publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc |
Citation | Oncogene, 2003, v. 22 n. 14, p. 2143-2150 How to Cite? |
Abstract | Resveratrol, a constituent of grapes and other foods, has been reported to be a potential cancer chemopreventive agent. Our previous study showed that the antitumor activity of resveratrol occurs through mitogen-activated protein kinases-mediated p53 activation and induction of apoptosis. To develop more effective agents with fewer side effects for the chemoprevention of cancer, we investigated the effect of resveratrol and its structurally related derivatives on epidermal growth factor (EGF)-induced cell transformation. Our results provided the first evidence that one of the resveratrol derivatives exerted a more potent inhibitory effect than resveratrol on EGF-induced cell transformation, but had less cytotoxic effects on normal nontransformed cells. Compared to resveratrol, this compound also caused cell cycle arrest in the G1 phase, but did not induce p53 activation and apoptosis. Furthermore, this compound, but not resveratrol, markedly inhibited EGF-induced phosphatidylinositol-3 kinase (PI-3K) and Akt activation. Collectively, these data suggested that the higher antitumor effect of the compound compared to resveratrol, may act through a different mechanism by mainly targeting PI-3K/Akt signaling pathways. |
Persistent Identifier | http://hdl.handle.net/10722/178801 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 2.334 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | She, QB | en_US |
dc.contributor.author | Ma, WY | en_US |
dc.contributor.author | Wang, M | en_US |
dc.contributor.author | Kaji, A | en_US |
dc.contributor.author | Ho, CT | en_US |
dc.contributor.author | Dong, Z | en_US |
dc.date.accessioned | 2012-12-19T09:49:49Z | - |
dc.date.available | 2012-12-19T09:49:49Z | - |
dc.date.issued | 2003 | en_US |
dc.identifier.citation | Oncogene, 2003, v. 22 n. 14, p. 2143-2150 | en_US |
dc.identifier.issn | 0950-9232 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/178801 | - |
dc.description.abstract | Resveratrol, a constituent of grapes and other foods, has been reported to be a potential cancer chemopreventive agent. Our previous study showed that the antitumor activity of resveratrol occurs through mitogen-activated protein kinases-mediated p53 activation and induction of apoptosis. To develop more effective agents with fewer side effects for the chemoprevention of cancer, we investigated the effect of resveratrol and its structurally related derivatives on epidermal growth factor (EGF)-induced cell transformation. Our results provided the first evidence that one of the resveratrol derivatives exerted a more potent inhibitory effect than resveratrol on EGF-induced cell transformation, but had less cytotoxic effects on normal nontransformed cells. Compared to resveratrol, this compound also caused cell cycle arrest in the G1 phase, but did not induce p53 activation and apoptosis. Furthermore, this compound, but not resveratrol, markedly inhibited EGF-induced phosphatidylinositol-3 kinase (PI-3K) and Akt activation. Collectively, these data suggested that the higher antitumor effect of the compound compared to resveratrol, may act through a different mechanism by mainly targeting PI-3K/Akt signaling pathways. | en_US |
dc.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/onc | en_US |
dc.relation.ispartof | Oncogene | en_US |
dc.subject | Cell transformation | - |
dc.subject | Chemoprevention | - |
dc.subject | p53 | - |
dc.subject | PI-3K/Akt | - |
dc.subject | Resveratrol | - |
dc.subject | Resveratrol derivatives | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Anticarcinogenic Agents - Pharmacology | en_US |
dc.subject.mesh | Apoptosis - Drug Effects | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Cell Transformation, Neoplastic - Chemically Induced - Drug Effects | en_US |
dc.subject.mesh | Epidermal Growth Factor | en_US |
dc.subject.mesh | G1 Phase - Drug Effects | en_US |
dc.subject.mesh | Gene Expression Regulation | en_US |
dc.subject.mesh | Genes, P53 | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Stilbenes - Chemical Synthesis - Pharmacology | en_US |
dc.title | Inhibition of cell transformation by resveratrol and its derivatives: Differential effects and mechanisms involved | en_US |
dc.type | Article | en_US |
dc.identifier.email | Wang, M: mfwang@hku.hk | en_US |
dc.identifier.authority | Wang, M=rp00800 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1038/sj.onc.1206370 | en_US |
dc.identifier.pmid | 12687016 | - |
dc.identifier.scopus | eid_2-s2.0-0038297516 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0038297516&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 22 | en_US |
dc.identifier.issue | 14 | en_US |
dc.identifier.spage | 2143 | en_US |
dc.identifier.epage | 2150 | en_US |
dc.identifier.isi | WOS:000182066900008 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | She, QB=7004176131 | en_US |
dc.identifier.scopusauthorid | Ma, WY=36071951400 | en_US |
dc.identifier.scopusauthorid | Wang, M=7406691844 | en_US |
dc.identifier.scopusauthorid | Kaji, A=36902726600 | en_US |
dc.identifier.scopusauthorid | Ho, CT=7404652573 | en_US |
dc.identifier.scopusauthorid | Dong, Z=7402274347 | en_US |
dc.identifier.issnl | 0950-9232 | - |