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Carcinogenesis Advance Access published online on November 20, 2006
Carcinogenesis, doi:10.1093/carcin/bgl221
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received January 18, 2006
Revised November 2, 2006
Accepted November 6, 2006

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Silibinin suppresses human osteosarcoma MG-63 cell invasion by inhibiting the ERK-dependent c-Jun/AP-1 induction of MMP-2

Yih-Shou Hsieh 1, Shu-Chen Chu 2, Shun-Fa Yang 3, Pei-Ni Chen 1, Yu-Chuan Liu 1, and Ko-Hsiu Lu 4 *

1 Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan
2 Department of Food Science, Central Taiwan University of Science and Technology, Taichung, Taiwan
3 Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
4 Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan; Department of Orthopaedic Surgery, Chung Shan Medical University Hospital, Chung Shan Medical University, Taichung 402, Taiwan

* To whom correspondence should be addressed.
Ko-Hsiu Lu, E-mail: cshy307{at}csh.org.tw


  Abstract

Silibinin is a natural flavonoid antioxidant with antihepatotoxic properties and pleiotropic anticancer capabilities. We tested the hypothesis that silibinin inhibits cellular invasiveness by downregulating the focal adhesion kinase (FAK) and extracellular signal-regulated protein kinases (ERKs)-dependent c-Jun/activator-protein-1 (AP-1) induction, which leads to inhibition of urokinase-type plasminogen activator (u-PA) and matrix metalloproteinase-2 (MMP-2) expressions in human osteoscarcoma MG-63 cells. We found that silibinin decreased cell adhesion and invasiveness, as well as inhibited u-PA and MMP-2 expressions. Silibinin reduced ERK 1/2 phosphorylation, but had no effects on the phosphorylation of c-Jun N-terminal kinases (JNK) 1/2, p38, and Akt. Silibinin suppressed AP-1 binding activity and c-Jun levels and its phosphorylation without changes of c-Fos and Ets-1 levels. Silibinin also inhibited interleukin-6 induced ERK1/2 and c-Jun phosphorylation, and cell invasiveness. Thus, silibinin may possess an anti-metastatic activity in MG-63 cells.

Keywords: silibinin; osteosarcoma MG-63; invasion; IL-6; MMP-2.
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