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Cancer chemopreventive and therapeutic potential of resveratrol: Mechanistic perspectives

DC Field Value Language
dc.contributor.authorKundu, Joydeb Kumar-
dc.contributor.authorSurh, Young-Joon-
dc.date.accessioned2021-01-31T10:16:40Z-
dc.date.available2021-01-31T10:16:40Z-
dc.date.created2017-11-15-
dc.date.issued2008-10-
dc.identifier.citationCancer Letters, Vol.269 No.2, pp.243-261-
dc.identifier.issn0304-3835-
dc.identifier.other3076-
dc.identifier.urihttps://hdl.handle.net/10371/172779-
dc.description.abstractA plant kingdom is considered as a gold mine for the discovery of many biologically active substances with therapeutic values. Resveratrol (3,5,4'-trihydroxystilbene), a naturally occurring polyphenol, exhibits pleiotropic health beneficial effects including anti-oxidant, anti-inflammatory, cardioprotective and anti-tumor activities. Currently, numerous preclinical findings suggest resveratrol as a promising nature's arsenal for cancer prevention and treatment. A remarkable progress in dissecting the molecular mechanisms underlying anti-cancer properties of resveratrol has been achieved in the past decade. As a potential anti-cancer agent, resveratrol has been shown to inhibit or retard the growth of various cancer cells in culture and implanted tumors in vivo. The compound significantly inhibits experimental tumorigenesis in a wide range of animal models. Resveratrol targets many components of intracellular signaling pathways including pro-inflammatory mediators, regulators of cell survival and apoptosis, and tumor angiogenic and metastatic switches by modulating a distinct set of upstream kinases, transcription factors and their regulators. This review summarizes the diverse molecular targets of resveratrol with a special focus on those involved in fine-tuning of orchestrated intracellular signal transduction. (C) 2008 Elsevier Ireland Ltd. All rights reserved.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleCancer chemopreventive and therapeutic potential of resveratrol: Mechanistic perspectives-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1016/j.canlet.2008.03.057-
dc.citation.journaltitleCancer Letters-
dc.identifier.wosid000260143500006-
dc.identifier.scopusid2-s2.0-51349132313-
dc.citation.endpage261-
dc.citation.number2-
dc.citation.startpage243-
dc.citation.volume269-
dc.identifier.sci000260143500006-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorSurh, Young-Joon-
dc.type.docTypeReview-
dc.description.journalClass1-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusHUMAN BREAST-CANCER-
dc.subject.keywordPlusMAMMARY EPITHELIAL-CELLS-
dc.subject.keywordPlusINHIBITS PHORBOL ESTER-
dc.subject.keywordPlusNITRIC-OXIDE SYNTHASE-
dc.subject.keywordPlusCARCINOMA A431 CELLS-
dc.subject.keywordPlusS-PHASE ARREST-
dc.subject.keywordPlusENDOTHELIAL GROWTH-FACTOR-
dc.subject.keywordPlusMOUSE SKIN TUMORIGENESIS-
dc.subject.keywordPlusDEXTRAN SODIUM-SULFATE-
dc.subject.keywordAuthorResveratrol-
dc.subject.keywordAuthorChemoprevention-
dc.subject.keywordAuthorSignal transduction-
dc.subject.keywordAuthorPhytochemicals-
dc.subject.keywordAuthorAnti-carcinogenesis-
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  • College of Pharmacy
  • Department of Pharmacy
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