This article was published online on 10 October 2013. Error was subsequently identified in the author correspondence. This notice is included in the online and print versions to indicate that both have been corrected [13 December 2013].
Chrysin inhibits metastatic potential of human triple-negative breast cancer cells by modulating matrix metalloproteinase-10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway†
Article first published online: 10 OCT 2013
Copyright © 2013 John Wiley & Sons, Ltd.
Journal of Applied Toxicology
Volume 34, Issue 1, pages 105–112, January 2014
How to Cite
Yang, B., Huang, J., Xiang, T., Yin, X., Luo, X., Huang, J., Luo, F., Li, H., Li, H. and Ren, G. (2014), Chrysin inhibits metastatic potential of human triple-negative breast cancer cells by modulating matrix metalloproteinase-10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway. J. Appl. Toxicol., 34: 105–112. doi: 10.1002/jat.2941
- Issue published online: 29 OCT 2013
- Article first published online: 10 OCT 2013
- Manuscript Accepted: 6 SEP 2013
- Manuscript Revised: 25 AUG 2013
- Manuscript Received: 5 JUN 2013
- National Natural Science Foundation of China. Grant Number: 81102007
- breast cancer;
- matrix metalloproteinase;
- epithelial-mesenchymal transition;
- phosphatidylinositol 3-kinase
Chrysin, a naturally occurring flavone, has been shown to inhibit cell proliferation and induce cell apoptosis in various cancers. However, the effect and mechanisms of chrysin on cancer metastasis are still enigmatic. In this study, metastatic triple-negative breast cancer (TNBC) cell lines were used to evaluate the antimetastatic activity of chrysin. The results showed that chrysin (5, 10 and 20 μM) significantly suppressed TNBC cell migration and invasion in a dose-dependent manner. Human matrix metalloproteinase (MMP) antibody array demonstrated that MMP-10 was downregulated by chrysin, which was further verified by Western blotting and ELISA. Moreover, it was shown that chrysin induced increased E-cadherin expression and decreased expression of vimentin, snail and slug in TNBC cells, suggesting that chrysin had a reversal effect on epithelial–mesenchymal transition. More importantly, it was demonstrated that inhibiting the Akt signal pathway might play a central role in chrysin-induced antimetastatic activity by regulating MMP-10 and epithelial–mesenchymal transition. In conclusion, our study indicates that chrysin exerts antimetastatic activities in TNBC cells, which suggests that chrysin might be a potential therapeutic candidate for the treatment of advanced or metastatic breast cancer. Copyright © 2013 John Wiley & Sons, Ltd.