Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/88346
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dc.contributorChinese Mainland Affairs Office-
dc.contributorDepartment of Applied Biology and Chemical Technology-
dc.creatorQu, Z-
dc.creatorLin, Y-
dc.creatorMok, DKW-
dc.creatorBian, Q-
dc.creatorTai, WCS-
dc.creatorChen, S-
dc.date.accessioned2020-10-29T01:02:36Z-
dc.date.available2020-10-29T01:02:36Z-
dc.identifier.urihttp://hdl.handle.net/10397/88346-
dc.language.isoenen_US
dc.publisherIvyspring Internationalen_US
dc.rights© The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.en_US
dc.rightsThe following publication Qu Z, Lin Y, Mok DKW, Bian Q, Tai WCS, Chen S. Arnicolide D Inhibits Triple Negative Breast Cancer Cell Proliferation by Suppression of Akt/mTOR and STAT3 Signaling Pathways. Int J Med Sci 2020; 17(11):1482-1490, is available at https://doi.org/10.7150/ijms.46925en_US
dc.subjectAkt/mTORen_US
dc.subjectArnicolide Den_US
dc.subjectSTAT3en_US
dc.subjectTriple negative breast canceren_US
dc.titleArnicolide D inhibits triple negative breast cancer cell proliferation by suppression of akt/mTOR and STAT3 signaling pathwaysen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1482-
dc.identifier.epage1490-
dc.identifier.volume17-
dc.identifier.issue11-
dc.identifier.doi10.7150/ijms.46925-
dcterms.abstractTriple-Negative Breast Cancer (TNBC) is a most dangerous breast cancer subtype. The naturally occurring sesquiterpene lactone, arnicolide D (AD), has proven effective against a variety of tumors, however, the inhibitory effects of AD against TNBC and the underlying mechanisms remain unclear. In the present study, two TNBC cell lines (MDA-MB-231 and MDA-MB-468) and an MDA-MB-231 xenograft mouse model were employed to investigate the anti-TNBC effects of AD in vitro and in vivo. Cell viability was assessed by MTT assay. Cell cycle arrest and apoptosis were analyzed by flow cytometry. Protein levels were determined by immunoblotting. In vitro studies demonstrated that AD significantly decreased cell viability, and induced G2/M cell cycle arrest and apoptosis. In vivo assays showed that oral administration of 25 or 50 mg/kg AD for 22 days led to a reduction of tumor weights by 24.7% or 41.0%, without appreciable side effects. Mechanistically, AD inhibited the activation of Akt/mTOR and STAT3 signaling pathways. Based on our findings, AD is a promising candidate for development as an adjunctive therapeutic drug for TNBC.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationInternational Journal of medical sciences, 2020, v. 17, no. 11, p. 1482-1490-
dcterms.isPartOfInternational Journal of medical sciences-
dcterms.issued2020-
dc.identifier.scopus2-s2.0-85087922549-
dc.identifier.pmid32669950-
dc.identifier.eissn1449-1907-
dc.description.validate202010 bcma-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOSen_US
dc.description.pubStatusPublisheden_US
dc.description.oaCategoryCCen_US
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