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      Hypaconitine inhibits TGF- β1-induced epithelial–mesenchymal transition and suppresses adhesion, migration, and invasion of lung cancer A549 cells

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          Abstract

          Epithelial-mesenchymal transition (EMT) has been implicated in tumor invasion and metastasis and provides novel strategies for cancer therapy. Hypaconitine (HpA), a diester-diterpenoid alkaloid isolated from the root of the Aconitum species, exhibits anti-inflammatory, analgesic, and especially, cardiotoxic activities. Here, we reported the anti-metastatic potentials of HpA in transforming growth factor- β1 (TGF- β1)-induced EMT in lung cancer A549 cells. The cytotoxic effect of HpA was determined by MTT assay. A549 cells were treated with TGF- β1 with or without HpA co-treatment, and the morphological alterations were observed with a microscopy. The expression of E-cadherin, N-cadherin, and NF-κB was determined by both Western blotting and immunofluorescence analyses. The adhesion, migration, and invasion were detected with Matrigel, wound-healing, and transwell assays, respectively. The expression of Snail was determined by Western blotting. The expression of NF- κB p65, I κBα, and p-I κBα in nuclear and cytosolic extracts was assessed by Western blotting. The results showed that low concentration of HpA (<16 μmol·L −1) had no obvious cytotoxicity to A549 cells. Morphologically, TGF- β1 treatment induced spindle-shaped alteration in the cells. The upregulation of N-cadherin, NF- κB, and Snail and the downregulation of E-cadherin were detected after TGF- β1 treatment. The adhesion, migration and invasion abilities were also increased by TGF- β1. Besides, TGF- β1 induced expression of Snail in a time-dependent manner. Furthermore, TGF- β1 induced nuclear translocation of NF- κB p65. All these alterations were dramatically inhibited by HpA co-treatment. In addition, the NF- κB inhibitor PDTC showed similar inhibitory effect. In conclusion, these results showed that HpA inhibited TGF- β1-induced EMT in A549 cells, which was possibly mediated by the inactivation of the NF- κB signaling pathway, providing an evidence for anti-cancer effect of HpA.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 June 2017
          : 15
          : 6
          : 427-435
          Affiliations
          1State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, China
          Author notes
          *Corresponding author: CHEN Xiu-Ping, Tel: +853-88224679, Fax: +853-28841358; E-mail: xpchen@ 123456umac.mo

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(17)30064-X
          10.1016/S1875-5364(17)30064-X
          Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: Science and Technology Development Fund (FDCT)
          Award ID: 039/2014/A1
          This work was supported by the Science and Technology Development Fund (FDCT), Macau SAR (039/2014/A1) and Research Fund of University of Macau (CPG2014-00012-ICMS).

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