Format

Send to

Choose Destination
J Ethnopharmacol. 2009 Nov 12;126(2):252-7. doi: 10.1016/j.jep.2009.08.032. Epub 2009 Aug 26.

Silibinin prevents TPA-induced MMP-9 expression by down-regulation of COX-2 in human breast cancer cells.

Author information

1
Department of Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Kangnam-gu, Seoul 135-710, South Korea.

Abstract

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 (MEK 1/2 inhibitor).

CONCLUSION:

Silibinin down-regulates TPA-induced MMP-9 expression through inhibition of COX-2 expression in breast cancer cells.

PMID:
19715751
DOI:
10.1016/j.jep.2009.08.032
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center