期刊
MOLECULES
卷 24, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/molecules24081584
关键词
brassinin; EMT; lung carcinoma; PI3K; Akt; mTOR
资金
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [NRF-2018R1D1A1B07042969, 2017M3A9E4065333]
- National Research Foundation of Korea [2017M3A9E4065333] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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.
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