Anti-cancer mechanism of arctigenin (ARC) in human lung cancer cells

dc.contributor.advisorLee, Seong-Hoen_US
dc.contributor.authorXu, Yanruien_US
dc.contributor.departmentNutritionen_US
dc.contributor.publisherDigital Repository at the University of Marylanden_US
dc.contributor.publisherUniversity of Maryland (College Park, Md.)en_US
dc.date.accessioned2018-09-12T05:32:10Z
dc.date.available2018-09-12T05:32:10Z
dc.date.issued2018en_US
dc.description.abstractArctigenin (ARC) is a lignan and is abundant in Asteraceae plant which possesses anti-inflammatory and anti-cancer activities. The current study was performed to investigate if ARC affects cancer progression and metastasis focusing on epithelial–mesenchymal transition (EMT) using invasive human lung cancer cell line, A549. No toxicity was observed in the cells treated with different doses of ARC (12-100 µM). The treatment of ARC repressed TGF-β-stimulated changes of metastatic morphology and cell invasion and migration. ARC inhibited TGF-β-induced phosphorylation and transcriptional activity of SMAD2/3 and expression of snail in dose-dependent and time-dependent manners. ARC also decreased expression of N-cadherin and increased expression of E-cadherin in dose-dependent and time-dependent manners. These changes were accompanied with decreased amount of nuclear phospho-SMAD2 and SMAD3, and nuclear translocation of SMAD2 and SMAD3. Moreover, ARC repressed TGF-β-induced phosphorylation of ERK. Our data demonstrate anti-metastatic activity of ARC in lung cancer model. Key words: ARC, TGF-β, EMT, Lung canceren_US
dc.identifierhttps://doi.org/10.13016/M22B8VG1V
dc.identifier.urihttp://hdl.handle.net/1903/21199
dc.language.isoenen_US
dc.subject.pqcontrolledNutritionen_US
dc.subject.pquncontrolledarctigeninen_US
dc.subject.pquncontrolledEMTen_US
dc.subject.pquncontrolledlung canceren_US
dc.subject.pquncontrolledTGF-βen_US
dc.titleAnti-cancer mechanism of arctigenin (ARC) in human lung cancer cellsen_US
dc.typeThesisen_US

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