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Chitosan-based nanoparticles with damnacanthal suppress CRM1 expression

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dc.contributor.authorChaichanasak, Nadda-
dc.contributor.authorRojanapanthu, Pleumchitt-
dc.contributor.authorYoon, Yongdae-
dc.contributor.authorGritsanapan, Wandee-
dc.contributor.authorChirachanchai, Suwabun-
dc.contributor.authorSathirakul, Korbtham-
dc.contributor.authorNualsanit, Thararat-
dc.contributor.authorSeong, Je Kyung-
dc.contributor.authorBaek, Seung Joon-
dc.date.accessioned2024-08-08T01:30:52Z-
dc.date.available2024-08-08T01:30:52Z-
dc.date.created2019-07-01-
dc.date.created2019-07-01-
dc.date.issued2018-12-
dc.identifier.citationOncology Letters, Vol.16 No.6, pp.7029-7034-
dc.identifier.issn1792-1074-
dc.identifier.urihttps://hdl.handle.net/10371/206364-
dc.description.abstractCancer is one of the leading causes of mortality worldwide. Phytochemicals may be promising anticancer agents given their various chemical structures and diverse biological activities. Damnacanthal (DAM) is a major bioactive component of Noni, which has been investigated previously as a cancer-preventive or chemotherapeutic agent. DAM has also been reported to exhibit anti-proliferative activity in several cancer types. In the present study, it was identified that DAM downregulates chromosome maintenance protein 1 (CRM1) expression in human cancer cells. The application of chitosan-based nanoparticles (NPs) with DAM also induced CRM1 downregulation, which suggests that chitosan-based NPs may be effective vehicles for delivery of phytochemicals such as DAM. It was also identified that DAM increased the levels of the tumor suppressor non-steroidal anti-inflammatory drugs-activated gene 1 in the nucleus, thereby leading to enhanced anticancer effects. The results of the present study indicate that DAM and its nanoformulation may be a candidate anticancer drug.-
dc.language영어-
dc.publisherSpandidos Publications-
dc.titleChitosan-based nanoparticles with damnacanthal suppress CRM1 expression-
dc.typeArticle-
dc.identifier.doi10.3892/ol.2018.9507-
dc.citation.journaltitleOncology Letters-
dc.identifier.wosid000451400400017-
dc.identifier.scopusid2-s2.0-85055205421-
dc.citation.endpage7034-
dc.citation.number6-
dc.citation.startpage7029-
dc.citation.volume16-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorSeong, Je Kyung-
dc.contributor.affiliatedAuthorBaek, Seung Joon-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusNUCLEAR EXPORT-
dc.subject.keywordPlusANTICANCER ACTIVITY-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusPOTENT-
dc.subject.keywordPlusP53-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusINDUCER-
dc.subject.keywordPlusKINASE-
dc.subject.keywordAuthordamnacanthal-
dc.subject.keywordAuthorchromosome maintenance protein 1-
dc.subject.keywordAuthornanoparticles-
dc.subject.keywordAuthorchitosan-
dc.subject.keywordAuthornon-steroidal anti-inflammatory drugs-activated gene-
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