期刊
BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
卷 25, 期 23, 页码 5508-5513出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bmcl.2015.10.067
关键词
Sanguiin H6; Epithelial-mesenchymal transition (EMT); Transforming growth factor-beta 1 (TGF-beta 1); Smad2/3 signaling pathway; Lung cancer; Migration; Invasion
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education, Science and Technology (MEST) [NRF-2013R1A1A2059010]
- Medical Research Center Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [2008-0062286]
- National Research Council of Science & Technology (NST), Republic of Korea [E0150300, E0150300-01] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
In the epithelial-mesenchymal transition (EMT), an important cellular process, epithelial cells become mesenchymal cells. This process is also critically involved in cancer metastasis. Sanguiin H6 is a compound derived from ellagitannin, which is found in berries. Sanguiin H6 shows various pharmacological properties, including anti-angiogenic activity. Because the possible role of sanguiin H6 in the EMT and the underlying molecular mechanisms are unclear, we investigated the effect of sanguiin H6 on the EMT. Transforming growth factor-beta 1 (TGF-beta 1) induces the EMT and promotes lung adenocarcinoma migration and invasion through the Smad2/3 signaling pathway. Thus, to understand the inhibitory effects of sanguiin H6 on lung cancer migration and invasion, we investigated the ability of sanguiin H6 to inhibit TGF-beta 1-induced EMT in the A549 cell line. We found that sanguiin H6 significantly prevented the activation of Smad2/3 signaling pathway by TGF-beta 1. Additionally, sanguiin H6 increased the expression of the epithelial marker E-cadherin and repressed the expression of Snail and the mesenchymal marker N-cadherin during TGF-beta 1-induced EMT. Moreover, sanguiin H6 regulated the expression of EMT-dependent genes induced by TGF-beta 1. Finally, sanguiin H6 inhibited the migration and invasion of TGF-beta 1-stimulated A549 cells. Taken together, our findings provide new evidence that sanguiin H6 suppresses lung cancer migration and invasion in vitro by inhibiting TGF-beta 1 induction of the EMT. (C) 2015 Published by Elsevier Ltd.
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