Green tea polyphenol (−)-epigallocatechin 3-gallate inhibits MMP-2 secretion and MT1-MMP-driven migration in glioblastoma cells

Annabi, Borhane; Lachambre, Marie-Paule; Bousquet-Gagnon, Nathalie; Pagé, Martine; Gingras, Denis; Béliveau, Richard

doi:10.1016/s0167-4889(01)00187-2

Cited by 156 publications

(101 citation statements)

References 46 publications

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“…28 Inhibition of MMPs has also been reported in several studies of phenolics compounds from green tea. [29][30][31] The reduction in total cell number in the Matrigel invasion assay was not due to cytotoxicity, as demonstrated in cell viability study (data not shown). In the assay of cell attachment to plastic substrate, there were no significant effects of either OVP or the isolated phenolics (data not shown).…”

Section: Discussionsupporting

confidence: 54%

Inhibitory effects of olive oil phenolics on invasion in human colon adenocarcinoma cells in vitro

Hashim

Rowland

McGlynn

et al. 2007

Intl Journal of Cancer

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Studies in human, animal and cellular systems suggest that phenols from virgin olive oil are capable of inhibiting several stages in carcinogenesis, including metastasis. The invasion cascade comprises cell attachment to extracellular matrix components or basement membrane, degradation of basement membrane by proteolytic enzymes and migration of cells through the modified matrix. In the present study, we investigated the effect of phenolics extracted from virgin olive oil (OVP) and its main constituents: hydroxytyrosol (3,4-dihydroxyphenylethanol), tyrosol (p-hydroxyphenylethanol), pinoresinol and caffeic acid. The effects of these phenolics were tested on the invasion of HT115 human colon carcinoma cells in a Matrigel invasion assay. OVP and its compounds showed different dose-related anti-invasive effects. At 25 lg/ml OVP and equivalent doses of individual compounds, significant anti-invasive effects were seen in the range of 45-55% of control. Importantly, OVP, but not the isolated phenolics, significantly reduced total cell number in the Matrigel invasion assay. There were no significant effects shown on cell viability, indicating the reduction of cell number in the Matrigel invasion assay was not due to cytotoxicity. There were also no significant effects on cell attachment to plastic substrate, indicating the importance of extracellular matrix in modulating the anti-invasive effects of OVP. In conclusion, the results from this study indicate that phenols from virgin olive oil have the ability to inhibit invasion of colon cancer cells and the effects may be mediated at different levels of the invasion cascade. ' 2007 Wiley-Liss, Inc.Key words: olive oil phenolics; colorectal cancer; invasion; adhesion; extracellular matrix In 2002, world cancer statistics for new colorectal cancer (CRC) cases were estimated to be more than 1 million, with more than 500,000 mortality cases. 1 Surgical resection is an effective treatment for localized disease, achieving a 5-year survival rate of 90%, but other normal treatments for metastatic disease remain ineffective. 2 Mediterranean countries have lower rates of CRC than other Western countries. 3 This has been attributed to a number of factors, one of which is consumption of olive oil. 3,4 Recently, olive oil phenolics have been shown to exert anticancer effects in a number of studies (reviewed in Refs. 5 and 6). Our previous study demonstrated that olive oil phenolics have the ability to inhibit initiation, promotion and invasion events in in vitro models of carcinogenesis. 7 Metastasis can be considered as a cascade of interrelated sequential steps. Cells must be able to disseminate from the primary tumor, invade the surrounding tissue, enter the circulatory system, evade immune responses, arrest at and colonize a distant site. 8 A 3-step hypothesis has been proposed to describe invasion of tumor cells: attachment to basement membrane or extracellular matrices (ECM), protease activity that induces local degradation of the matrix, and migration of tumor cells through the...

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Section: Discussionsupporting

confidence: 54%

Inhibitory effects of olive oil phenolics on invasion in human colon adenocarcinoma cells in vitro

Hashim

Rowland

McGlynn

et al. 2007

Intl Journal of Cancer

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“…One common intracellular pathway may also involve Ca 2ϩ /calmodulin-dependent signaling, which has been shown to regulate MT1-MMP cell surface processing (25), as well as the phosphorylation of CD44 required for cell migration on HA (62). Finally, we also report that EGCg, an effective inhibitor of MT1-MMP-mediated functions (36,63), also antagonized MT1-MMP-mediated cell surface HA-binding.…”

Section: Discussionmentioning

confidence: 51%

“…C, carbonate extraction was performed as described under "Experimental Procedures"; lysates were fractionated in a discontinuous sucrose density gradient. anti-angiogenic and anti-MMP inhibitory activities (35)(36)(37). We demonstrated that HA cell surface binding in control glioma cells treated for 1 h with either ilomastat or EGCg had no effect (Fig.…”

Section: Cholesterol Depletion Increases the Cell Surface Binding Of mentioning

confidence: 90%

Hyaluronan Cell Surface Binding Is Induced by Type I Collagen and Regulated by Caveolae in Glioma Cells

Annabi

Thibeault

Moumdjian

et al. 2004

Journal of Biological Chemistry

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Hyaluronan (HA) is a component of the brain extracellular matrix environment that is synthesized and secreted by glioma cells. The primary cell surface receptor for HA is CD44, a membrane glycoprotein that is functionally regulated by a membrane type 1 matrix metalloproteinase (MT1-MMP). Both CD44 and MT1-MMP are partially located in Triton X-100-insoluble domains, but no functional link has yet been established between them. In the present study, we studied the regulation of HA cell surface binding in U-87 glioma cells. We show that an MMP-dependent mechanism regulates the intrinsic cell surface binding of HA as ilomastat, a broad MMP inhibitor, increased HA binding to glioma cells. HA binding was also rapidly and specifically up-regulated by 3-fold by type I collagen in U-87 cells, which also induced a significant morphological reorganization associated with the activation of a latent form of MMP-2 through a MT1-MMP-mediated mechanism. Interestingly, caveolae depletion with a cell surface cholesteroldepleting agent ␤-cyclodextrin triggered an additional increase (9-fold) in the binding of HA, in synergy with type I collagen. On the other hand, HA cell surface binding was diminished by the MEK inhibitor PD98059 and by the overexpression of a recombinant, wild type MT1-MMP, whereas its cytoplasmic-deleted form had no effect. Taken together, our results suggest that MT1-MMP regulates, through its cytoplasmic domain, the cell surface functions of CD44 in a collagen-rich pericellular environment. Additionally, we describe a new molecular mechanism regulating the invasive potential of glioma cells involving a MT1-MMP/CD44/caveolin interaction, which could represent a potential target for anti-cancer therapies.The principal molecules that have been identified in the normal brain extracellular matrix (ECM) 1 are hyaluronan (HA; also known as hyaluronic acid, hyaluronate) and chondroitin sulfate (1, 2). HA is an important glycosaminoglycan constituent believed to be implicated in angiogenesis, the formation of new blood vessels from preexisting vasculature. Although the serum level of HA is already used as an indicator of progressive malignant disease (3), its effects on in vivo angiogenesis and endothelial cell (EC) function are complex and have been reported to depend on HA concentration and molecular size (4, 5). Accordingly, whereas high molecular weight HA was shown to inhibit EC functions (6), low molecular weight HA stimulated EC proliferation, tubulogenesis (6, 7), and neovascularization (8). Moreover, small HA polymers efficiently regulated CD44 cell surface functional expression and promoted tumor cell migration (9). Astrocytic tumors of the central nervous system express CD44 among other cell adhesion receptors of the integrin or immunoglobulin superfamily. Although HA is the principal ligand of CD44, other CD44 ligands include the ECM components collagen, fibronectin, laminin, and chondroitin sulfate, whereas mucosal addressin, serglycin, osteopontin, and the class II invariant chain represent ECM-unrelat...

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“…(Ϫ)Epigallocatechin-3-gallate (EGCG) is the major bioactive polyphenol present in green tea. It possesses anti-oxidant (16), anti-mutagenic (17), anti-proteolytic (18,19), and anti-proliferative activity (20). In addition, it has been shown to increase p27 KIP-1 levels, inhibit cyclin activity, and inhibit cell cycle progression (21,22).…”

mentioning

confidence: 99%

Epigallocatechin-3-gallate Inhibits Epidermal Growth Factor Receptor Signaling Pathway

Sah

Balasubramanian

Eckert

et al. 2004

Journal of Biological Chemistry

238

143

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Epidermal growth factor receptor (EGFR) activation is absolutely required for cervical cell proliferation. This suggests that EGFR-inhibitory agents may be of therapeutic value. In the present study, we investigated the effects of epigallocatechin-3-gallate (EGCG), a bioactive green tea polyphenol, on EGFR signaling in cervical cells. EGCG inhibits epidermal growth factor-dependent activation of EGFR, and EGFR-dependent activation of the mitogen-activated protein kinases ERK1/2. EGCG also inhibits EGFR-dependent AKT activity. The EGCGdependent reduction in ERK and AKT activity is associated with reduced phosphorylation of downstream substrates, including p90RSK, FKHR, and BAD. These changes are associated with increased p53, p21 WAF-1 , and p27 KIP-1 levels, reduced cyclin E level, and reduced CDK2 kinase activity. Consistent with these findings, flow cytometry and TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling) staining revealed EGCG-dependent G 1 arrest. Moreover, sustained EGCG treatment caused apoptotic cell death. In addition to inhibiting EGFR, cell-free studies demonstrated that EGCG directly inhibits ERK1/2 and AKT, suggesting that EGCG acts simultaneously at multiple levels to inhibit EGF-dependent signaling. Importantly, the EGCG inhibition is selective, as EGCG does not effect the EGFR-dependent activation of JNK. These results suggest that EGCG acts to selectively inhibit multiple EGF-dependent kinases to inhibit cell proliferation.

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Green tea polyphenol (−)-epigallocatechin 3-gallate inhibits MMP-2 secretion and MT1-MMP-driven migration in glioblastoma cells

Cited by 156 publications

References 46 publications

Inhibitory effects of olive oil phenolics on invasion in human colon adenocarcinoma cells in vitro

Inhibitory effects of olive oil phenolics on invasion in human colon adenocarcinoma cells in vitro

Hyaluronan Cell Surface Binding Is Induced by Type I Collagen and Regulated by Caveolae in Glioma Cells

Epigallocatechin-3-gallate Inhibits Epidermal Growth Factor Receptor Signaling Pathway

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