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Brassinin Represses Invasive Potential of Lung Carcinoma Cells through Deactivation of PI3K/Akt/mTOR Signaling Cascade

1
KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea
2
Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea
3
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore
*
Authors to whom correspondence should be addressed.
Academic Editor: Philippe Jeandet
Molecules 2019, 24(8), 1584; https://doi.org/10.3390/molecules24081584
Received: 15 April 2019 / Revised: 19 April 2019 / Accepted: 19 April 2019 / Published: 22 April 2019
(This article belongs to the Special Issue Discovery of Active Ingredients from Natural Products)
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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-β)-mediated regulation of diverse mesenchymal markers. Additionally, BSN did increase the expression of various epithelial marker proteins in lung cancer cells. TGF-β-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. View Full-Text
Keywords: brassinin; EMT; lung carcinoma; PI3K/Akt/mTOR brassinin; EMT; lung carcinoma; PI3K/Akt/mTOR
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Yang, M.H.; Lee, J.H.; Ko, J.-H.; Jung, S.H.; Sethi, G.; Ahn, K.S. Brassinin Represses Invasive Potential of Lung Carcinoma Cells through Deactivation of PI3K/Akt/mTOR Signaling Cascade. Molecules 2019, 24, 1584.

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