Please use this identifier to cite or link to this item: https://doi.org/10.3390/molecules24081584
DC FieldValue
dc.titleBrassinin represses invasive potential of lung carcinoma cells through deactivation of PI3K/Akt/mTOR signaling cascade
dc.contributor.authorYang, M.H.
dc.contributor.authorLee, J.H.
dc.contributor.authorKo, J.-H.
dc.contributor.authorJung, S.H.
dc.contributor.authorSethi, G.
dc.contributor.authorAhn, K.S.
dc.date.accessioned2021-12-29T04:36:00Z
dc.date.available2021-12-29T04:36:00Z
dc.date.issued2019
dc.identifier.citationYang, M.H., Lee, J.H., Ko, J.-H., Jung, S.H., Sethi, G., Ahn, K.S. (2019). Brassinin represses invasive potential of lung carcinoma cells through deactivation of PI3K/Akt/mTOR signaling cascade. Molecules 24 (8) : 1584. ScholarBank@NUS Repository. https://doi.org/10.3390/molecules24081584
dc.identifier.issn14203049
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/212311
dc.description.abstractThe epithelial–mesenchymal transition (EMT) is a phenomenon that facilitates epithelial cells to acquire invasive potential to induce the initiation the metastatic spread of tumor cells. Here, we determined if brassinin (BSN) can affect the EMT process and deciphered its anti-cancer effects. BSN attenuated the levels of EMT linked genes and suppressed transforming growth factor beta (TGF-?)-mediated regulation of diverse mesenchymal markers. Additionally, BSN did increase the expression of various epithelial marker proteins in lung cancer cells. TGF-?-induced morphological changes and induction of invasive ability of tumor cells was also found to be abrogated by BSN treatment. Finally, BSN not only suppressed constitutive, but also inducible phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) phosphorylation in tumor cells. © 2019 by the authors.
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.sourceScopus OA2019
dc.subjectBrassinin
dc.subjectEMT
dc.subjectLung carcinoma
dc.subjectPI3K/Akt/mTOR
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.3390/molecules24081584
dc.description.sourcetitleMolecules
dc.description.volume24
dc.description.issue8
dc.description.page1584
Appears in Collections:Staff Publications
Elements

Show simple item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_3390_molecules24081584.pdf4.36 MBAdobe PDF

OPEN

NoneView/Download

Google ScholarTM

Check

Altmetric


This item is licensed under a Creative Commons License Creative Commons