Yang, Min Hee Lee, Jong Hyun Ko, Jeong-Hyeon Jung, Sang Hoon Sethi, Gautam Ahn, Kwang Seok 2024-01-19T20:04:58Z 2024-01-19T20:04:58Z 2021-08-31 2019-04-02 1420-3049 https://pubs.kist.re.kr/handle/201004/120115 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. English MDPI EPITHELIAL-MESENCHYMAL TRANSITION MOLECULAR-MECHANISMS CANCER METASTASIS EXPRESSION SUPPRESSION CHEMOSENSITIZATION ADENOCARCINOMA INHIBITION Brassinin Represses Invasive Potential of Lung Carcinoma Cells through Deactivation of PI3K/Akt/mTOR Signaling Cascade Article 10.3390/molecules24081584 1 MOLECULES, v.24, no.8 MOLECULES 24 8 scie scopus 000467765700139 2-s2.0-85064839489 Biochemistry & Molecular Biology Chemistry, Multidisciplinary Biochemistry & Molecular Biology Chemistry Article EPITHELIAL-MESENCHYMAL TRANSITION MOLECULAR-MECHANISMS CANCER METASTASIS EXPRESSION SUPPRESSION CHEMOSENSITIZATION ADENOCARCINOMA INHIBITION brassinin EMT lung carcinoma PI3K Akt mTOR