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Osthole inhibited TGF beta-induced epithelial-mesenchymal transition (EMT) by suppressing NF-kappa B mediated Snail activation in lung cancer A549 cells
Feng, Haitao1; Lu, Jin-Jian1; Wang, Yitao1; Pei, Lixia2; Chen, Xiuping1
2017
Source PublicationCELL ADHESION & MIGRATION
ISSN1933-6918
Volume11Issue:5-6Pages:464-475
Abstract

Epithelial-mesenchymal transition (EMT), the transdifferentiation of epithelial cells into mesenchymal cells, has been implicated in the metastasis and provides novel strategies for cancer therapy. Osthole (OST), a dominant active constituent of Chinese herb Cnidium monnieri, has been reported to inhibit cancer metastasis while the mechanisms remains unclear. Here, we studied the inhibitory effect and mechanisms of OST on TGF-beta 1-induced EMT in A549 cells. Cells were treated with TGF-beta 1 in the absence and presence of OST. The morphological alterations were observed with a microscopy. The protein and mRNA expressions were determined by Western blotting and real-time PCR. The protein localization was detected with immunofluorescence. The adhesion, migration, and invasion were determined by Matrigel, wound-healing, and Transwell assays. TGF-beta 1 treatment induced spindle-shaped alterations of cells, upregulation of N-cadherin, Vimentin, NF-kappa B p65, and downregulation of E-cadherin. Dysregulated membrane expression and mRNA expression of E-cadherin and N-cadherin were observed after TGF-beta 1 treatment. TGF-beta 1 increased abilities of migration and invasion and triggered the nuclear translocation of NF-kappa B p65. These alterations were dramatically inhibited by OST. Furthermore, PDTC, a NF-kappa B inhibitor, showed similar effects. In addition, TGF-beta 1-induced expression of Snail was significantly inhibited by OST and silenced Snail partially reversed TGF-beta 1-induced EMT biomarkers without affecting NF-kappa B p-65. In conclusion, OST inhibited TGF-beta 1-induced EMT, adhesion, migration, and invasion through inactivation of NF-kappa B-Snail pathways in A549 cells. This study provides novel molecular mechanisms for the anti-metastatic effect of OST.

KeywordEmt Nf-kappa b Osthole Snail Tgf-beta 1
DOIhttp://doi.org/10.1080/19336918.2016.1259058
URLView the original
Indexed BySCI
Language英语
WOS Research AreaCell Biology
WOS SubjectCell Biology
WOS IDWOS:000423046400004
PublisherTAYLOR & FRANCIS INC
The Source to ArticleWOS
Fulltext Access
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Cited Times [WOS]:18   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Affiliation1.State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, China
2.Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
First Author AffilicationInstitute of Chinese Medical Sciences
Recommended Citation
GB/T 7714
Feng, Haitao,Lu, Jin-Jian,Wang, Yitao,et al. Osthole inhibited TGF beta-induced epithelial-mesenchymal transition (EMT) by suppressing NF-kappa B mediated Snail activation in lung cancer A549 cells[J]. CELL ADHESION & MIGRATION,2017,11(5-6):464-475.
APA Feng, Haitao,Lu, Jin-Jian,Wang, Yitao,Pei, Lixia,&Chen, Xiuping.(2017).Osthole inhibited TGF beta-induced epithelial-mesenchymal transition (EMT) by suppressing NF-kappa B mediated Snail activation in lung cancer A549 cells.CELL ADHESION & MIGRATION,11(5-6),464-475.
MLA Feng, Haitao,et al."Osthole inhibited TGF beta-induced epithelial-mesenchymal transition (EMT) by suppressing NF-kappa B mediated Snail activation in lung cancer A549 cells".CELL ADHESION & MIGRATION 11.5-6(2017):464-475.
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