PMID- 31013639 OWN - NLM STAT- MEDLINE DCOM- 20190813 LR - 20211204 IS - 1420-3049 (Electronic) IS - 1420-3049 (Linking) VI - 24 IP - 8 DP - 2019 Apr 22 TI - Brassinin Represses Invasive Potential of Lung Carcinoma Cells through Deactivation of PI3K/Akt/mTOR Signaling Cascade. LID - 10.3390/molecules24081584 [doi] LID - 1584 AB - 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-beta)-mediated regulation of diverse mesenchymal markers. Additionally, BSN did increase the expression of various epithelial marker proteins in lung cancer cells. TGF-beta-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. FAU - Yang, Min Hee AU - Yang MH AD - KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea. didmini@naver.com. FAU - Lee, Jong Hyun AU - Lee JH AD - Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. mirue88@nate.com. FAU - Ko, Jeong-Hyeon AU - Ko JH AD - Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. gokjh1647@gmail.com. FAU - Jung, Sang Hoon AU - Jung SH AD - KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea. shjung507@gmail.com. FAU - Sethi, Gautam AU - Sethi G AD - Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117600, Singapore. phcgs@nus.edu.sg. FAU - Ahn, Kwang Seok AU - Ahn KS AUID- ORCID: 0000-0002-2882-0612 AD - KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Korea. ksahn@khu.ac.kr. AD - Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. ksahn@khu.ac.kr. LA - eng GR - NRF-2018R1D1A1B07042969 and 2017M3A9E4065333/National Research Foundation of Korea/ PT - Journal Article DEP - 20190422 PL - Switzerland TA - Molecules JT - Molecules (Basel, Switzerland) JID - 100964009 RN - 0 (Indoles) RN - 0 (Thiocarbamates) RN - 105748-59-2 (brassinin) RN - EC 2.7.1.1 (MTOR protein, human) RN - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) MH - A549 Cells MH - Epithelial-Mesenchymal Transition/*drug effects MH - Humans MH - Indoles/*pharmacology MH - Lung Neoplasms/*drug therapy/*metabolism/pathology MH - Phosphatidylinositol 3-Kinase/*metabolism MH - Proto-Oncogene Proteins c-akt/*metabolism MH - Signal Transduction/*drug effects MH - TOR Serine-Threonine Kinases/*metabolism MH - Thiocarbamates/*pharmacology PMC - PMC6514890 OTO - NOTNLM OT - EMT OT - PI3K/Akt/mTOR OT - brassinin OT - lung carcinoma COIS- The authors declare no conflict of interest. EDAT- 2019/04/25 06:00 MHDA- 2019/08/14 06:00 PMCR- 2019/04/22 CRDT- 2019/04/25 06:00 PHST- 2019/04/15 00:00 [received] PHST- 2019/04/19 00:00 [revised] PHST- 2019/04/19 00:00 [accepted] PHST- 2019/04/25 06:00 [entrez] PHST- 2019/04/25 06:00 [pubmed] PHST- 2019/08/14 06:00 [medline] PHST- 2019/04/22 00:00 [pmc-release] AID - molecules24081584 [pii] AID - molecules-24-01584 [pii] AID - 10.3390/molecules24081584 [doi] PST - epublish SO - Molecules. 2019 Apr 22;24(8):1584. doi: 10.3390/molecules24081584.