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Evidence-Based Complementary and Alternative Medicine
Volume 2018 (2018), Article ID 7202548, 15 pages
Research Article

Propolin C Inhibited Migration and Invasion via Suppression of EGFR-Mediated Epithelial-to-Mesenchymal Transition in Human Lung Cancer Cells

1Division of Hematology and Oncology, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan City, Taiwan
2Department of Nutritional Science, Fu Jen Catholic University, New Taipei City, Taiwan
3Graduate Institute of Natural Products, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
4Center for Traditional Chinese Medicine, Chang Gung Memorial Hospital, Taoyuan City, Taiwan

Correspondence should be addressed to Yann-Lii Leu and Meng-Shih Weng

Received 16 October 2017; Accepted 28 January 2018; Published 25 February 2018

Academic Editor: Marco F. L. Lemos

Copyright © 2018 Jih-Tung Pai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Controlling lung cancer cell migration and invasion via epithelial-to-mesenchymal transition (EMT) through the regulation of epidermal growth factor receptor (EGFR) signaling pathway has been demonstrated. Searching biological active phytochemicals to repress EGFR-regulated EMT might prevent lung cancer progression. Propolis has been used as folk medicine in many countries and possesses anti-inflammatory, antioxidant, and anticancer activities. In this study, the antimigration and anti-invasion activities of propolin C, a c-prenylflavanone from Taiwanese propolis, were investigated on EGFR-regulated EMT signaling pathway. Cell migration and invasion activities were dose-dependently suppressed by noncytotoxic concentration of propolin C. Downregulations of vimentin and snail as well as upregulation of E-cadherin expressions were through the inhibition of EGFR-mediated phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and extracellular signal-regulated kinase (ERK) signaling pathway in propolin C-treated cells. In addition, EGF-induced migration and invasion were suppressed by propolin C-treated A549 lung cancer cells. No significant differences in E-cadherin expression were observed in EGF-stimulated cells. Interestingly, EGF-induced expressions of vimentin, snail, and slug were suppressed through the inhibition of PI3K/Akt and ERK signaling pathway in propolin C-treated cells. Inhibition of cell migration and invasion by propolin C was through the inhibition of EGF/EGFR-mediated signaling pathway, followed by EMT suppression in lung cancer.