Please use this identifier to cite or link to this item: https://doi.org/10.3390/molecules24081584
Title: Brassinin represses invasive potential of lung carcinoma cells through deactivation of PI3K/Akt/mTOR signaling cascade
Authors: Yang, M.H.
Lee, J.H.
Ko, J.-H.
Jung, S.H.
Sethi, G. 
Ahn, K.S.
Keywords: Brassinin
EMT
Lung carcinoma
PI3K/Akt/mTOR
Issue Date: 2019
Publisher: MDPI AG
Citation: Yang, 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
Rights: Attribution 4.0 International
Abstract: The 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.
Source Title: Molecules
URI: https://scholarbank.nus.edu.sg/handle/10635/212311
ISSN: 14203049
DOI: 10.3390/molecules24081584
Rights: Attribution 4.0 International
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