期刊
JOURNAL OF ETHNOPHARMACOLOGY
卷 126, 期 2, 页码 252-257出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2009.08.032
关键词
Silibinin; TPA; MMP-9; COX-2; ERK
资金
- In-SUNG Foundation for Medical Research [C-A9-850-1]
- Korean Government [KRF-2009-0068603]
- [C-A9-851-1]
Ethnopharmacological relevance: The expression of matrix metalloproteinase-9 (MMP-9) and cyclooxygenase-2 (COX-2) are pivotal steps in breast cancer pathogenesis. In a previous study, we reported that silibinin suppresses TPA-induced MMP-9 expression through the Raf/MEK/ERK pathway. Aims of the study: Herein we determined the co-relationship between MMP-9 and COX-2, as well as the effect of silibinin on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced MMP-9 and COX-2 expression in the human breast cancer cells, MCF-7 and MDA-MB231. Methods: The toxicity of silibinin was evaluated by Quick Cell Proliferation Assay Kit II. MMP-9 and COX-2 expression were analyzed by Zymography and Western blotting, respectively. Adenoviral constitutively active (CA)-MEK was used to activate MEK/ERK pathway. Results: The expression of MMP-9 and COX-2 in response to TPA was increased, whereas TPA-induced MMP-9 and COX-2 expression was decreased by silibinin. Our results showed that TPA-induced MMP-9 expression was inhibited by celecoxib in a dose-dependent fashion, but not MMP-1-expression. Both MMP-9 and COX-2 expression were significantly increased by CA-MEK overexpression. In contrast, TPA-induced MMP-9 and COX-2 expression was decreased by UO126 (MEK1/2 inhibitor). Conclusion: Silibinin down-regulates TPA-induced MMP-9 expression through inhibition of COX-2 expression in breast cancer cells. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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