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Silymarin Attenuates Invasion and Migration through the Regulation of Epithelial-mesenchymal Transition in Huh7 Cells
Korean J Clin Lab Sci 2018;50:337-344  
Published on September 30, 2018
Copyright © 2018 Korean Society for Clinical Laboratory Science.

Do-Hoon Kim1, So-Jeong Park1, Seung-Yeon Lee1, Hyun-Seo Yoon2, Chung Mu Park1

1Department of Clinical Laboratory Science, Dong-Eui University, Busan, Korea
2Department of Dental Hygiene, Dong-Eui University, Busan, Korea
Correspondence to: Chung Mu Park
Department of Clinical Laboratory Science, Dong-Eui University, 176 Eomgwang-ro, Busanjin-gu, Busan 47340, Korea
Tel: 82-51-890-2685
Fax: 82-505-182-6877
E-mail: cmpark@deu.ac.kr
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Hepatocellular carcinoma (HCC), a major type of hepatoma, is associated with high recurrence and mortality because of its uncontrolled metastatic feature. Silymarin is a polyphenolic flavonoid from Silybum marianun (milk thistle) and exhibits anti-carcinogenic activity through modulation of the epithelial-mesenchymal transition (EMT) in several cancer cells. In this study, the inhibitory mechanism of silymarin against migration and invasion was investigated in the Huh7 HCC cell line. Wound healing and in vitro invasion assays were conducted to examine the effects of silymarin on migration and invasion. Western blot analysis was also applied to evaluate the inhibitory effects of silymarin on the EMT-related genes and their upstream signaling molecules. Silymarin inhibited the migratory and invasive activities of Huh7 cells. In addition, silymarin attenuated the protein expression levels of vimentin and matrix metalloproteinase (MMP)-9 as well as their transcription factors, Snail, and nuclear factor (NF)-κB, while the expression of E-cadherin was increased by the silymarin treatment. Among the upstream signaling molecules, the phosphorylation of Akt was inhibited by the silymarin treatment, which was confirmed by the selective inhibitor, LY294002. Consequently, silymarin inhibited the invasive and migratory activities in Huh7 cells through the modulation of EMT-related gene expression by the PI3K/Akt signaling pathway, which may have potential as a chemopreventive agent against HCC metastasis.
Keywords : Epithelial-mesenchymal transition, NF-kappa B, Silymarin, Snail family transcription factors

September 2018, 50 (3)
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