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Carcinogenesis Advance Access originally published online on April 28, 2005
Carcinogenesis 2005 26(9):1553-1562; doi:10.1093/carcin/bgi104
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Carcinogenesis vol.26 no.9 © Oxford University Press 2005; all rights reserved.

(–)-Epigallocatechin-3-gallate promotes pro-matrix metalloproteinase-7 production via activation of the JNK1/2 pathway in HT-29 human colorectal cancer cells

Mihye Kim, Akira Murakami, Kyuichi Kawabata and Hajime Ohigashi *

Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Kyoto 606-8502, Japan

* To whom correspondence should be addressed. Tel: +81 75 753 6281; Fax: +81 75 753 6284; Email: ohigashi{at}kais.kyoto-u.ac.jp

Matrix metalloproteinase (MMP)-7 (matrilysin-1) plays significant roles in the growth, invasion, and metastasis of colorectal tumors, while (–)-epigallocatechin-3-gallate (EGCG), a green tea polyphenol with chemopreventive properties, has been shown to be an inhibitor of MMP-2 and MMP-9. In the present study, HT-29 human colorectal cancer cells were treated with EGCG to examine its effects on pro-MMP-7 induction and production using RT–PCR and western blot analyses. Surprisingly, EGCG (10–100 µM) treatment increased both intracellular and extracellular pro-MMP-7 protein levels (2.6–8.4-fold and 1.9–6.4-fold, respectively) in dose- and time-dependent manner, with a significant upregulation of its mRNA expression. EGCG also activated extracellular signal-regulated protein kinase (ERK)1/2, c-JUN NH2-terminal kinase (JNK)1/2 and p38 mitogen-activated protein kinase (MAPK), as previously reported. In addition, the polyphenol triggered the phosphorylation of c-JUN (Ser63 and Ser73) and induced c-JUN/c-FOS, thereby increasing the DNA binding activity of activator protein-1 (AP-1), as shown by an AP-1 luciferase reporter assay. Pharmacological blockade of MAPK activities suggested that pro-MMP-7 expression was induced via JNK1/2 activation, but not in the case of ERK1/2 or p38 MAPK. N-Acetyl-L-cysteine, superoxide () dismutase and catalase attenuated the EGCG-induced pro-MMP-7 production, suggesting an involvement of oxidative stress in these events. Conversely, EGCG spontaneously generated in a cell-free system that utilized a cytochrome C reduction method. Further, (–)-epicatechin-3-gallate (25 and 100 µM) and green tea polyphenols (33 and 132 µg/ml) induced pro-MMP-7 expression, whereas (–)-epicatechin and (–)-epigallocatechin (100 µM each) did not. Induction of pro-MMP-7 expression by EGCG was also shown in another human colorectal adenocarcinoma cell line, Caco-2. Our results suggest that some green tea catechins induce pro-MMP-7 production via production and the activation of JNK1/2, c-JUN, c-FOS and AP-1 in HT-29 cells.


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