(−)-Epigallocatechin gallate inhibits membrane-type 1 matrix metalloproteinase, MT1-MMP, and tumor angiogenesis

Yamakawa, Satoru; Asai, Tomohiro; Uchida, Takayuki; Matsukawa, Motomi; Akizawa, Toshifumi; Oku, Naoto

doi:10.1016/j.canlet.2004.03.008

Cited by 76 publications

(53 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The initial antiangiogenic properties attributed to EA and EGCG (when incubated with non-conditioned media) are distinct from their increasing capacity to suppress the CD31 þ cell tubulogenesis promoted by increasing numbers of 435S cells, thus suggesting another mode of action. Given that EGCG has been shown to inhibit cancer-associated enzymes such as matrix metalloproteinases (MMPs) (Yamakawa et al, 2004) and the proteasome (Kazi et al, 2004), we suggest that EGCG and EA inhibition of secreted NDPK-B is another anticancer and antiangiogenic property that can be attributed to these polyphenolic compounds. We propose that EA's potency as an NDPK-B inhibitor and the subsequent reduction of extracellular ATP levels (Yang et al, 1994;Malmquist et al, 2001) may, in part explain why EA is a more potent inhibitor of CD31 þ cell tubulogenesis than is EGCG.…”

Section: Discussionmentioning

confidence: 82%

Purinergic regulation of angiogenesis by human breast carcinoma-secreted nucleoside diphosphate kinase

et al. 2007

View full text Add to dashboard Cite

MDA-MB-435S human breast cancer cells (435S) secrete nucleoside diphosphate kinase (NDPK) that supports metastases and is inhibited by epigallocatechin gallate (EGCG) and ellagic acid (EA). We hypothesise that 435S cell-secreted NDPK-B supports tumour formation by modulating ATP levels locally to activate endothelial cell (EC) P2Y receptor-mediated angiogenesis. Epigallocatechin gallate (IC 50 ¼ 8-10 mM) and EA (IC 50 ¼ 2-3 mM) suppressed 435S cell growth, but had less effect on human CD31 þ EC growth. Epigallocatechin gallate (IC 50 ¼ 11 mM) and EA (IC 50 ¼ 1 mM) also prevented CD31 þ EC tubulogenesis on Matrigelt. 435S cellconditioned media induced tubulogenesis in a cell number, time, and nucleotide-dependent manner. Ellagic acid (1 mM), but not equimolar EGCG, reduced cell number-dependent angiogenesis. P2Y 1 receptor activation by NDPK-generated nucleotide (100 mM ATP) or by 10 mM 2-methyl-thio-ATP (2MS-ATP) promoted tubulogenesis on collagen and was blocked by the P2Y 1 antagonist MRS2179 (10 mM). Physiological amounts of purified as well as 435S cell-secreted NDPK also promoted angiogenesis that was attenuated by NDPK depletion or 10 mM MRS2179, indicating a P2Y 1 receptor-mediated pathway. These results support the notion that secreted NDPK mediates angiogenesis via P2Y receptor signalling and suggests that novel inhibitors of NDPK may be useful as therapeutics.

show abstract

Section: Discussionmentioning

confidence: 82%

Purinergic regulation of angiogenesis by human breast carcinoma-secreted nucleoside diphosphate kinase

et al. 2007

View full text Add to dashboard Cite

show abstract

“…54 Epigallocatechin gallate, the chemopreventive component of green tea, inhibits membrane-type 1 matrix metalloproteinase and tumor angiogenesis. 55,56 PLAU is responsible for the activation of plasminogen. Thrombospondin (THBS1) and Ephrin A2 represent endogenous angiogenesis inhibitors, 57,58 whose expression also correlated with cellular response to ARSs in our analysis.…”

Section: Discussionmentioning

confidence: 99%

Microarray expression profiles of angiogenesis-related genes predict tumor cell response to artemisinins

et al. 2006

View full text Add to dashboard Cite

Artemisinin (ARS) and its derivatives are used for the second-line therapy of malaria infections with Plasmodium falciparum and P. vivax. ARSs also reveal profound antitumor activity in vitro and in vivo. In the present investigation, we correlated the mRNA expression data of 89 angiogenesis-related genes obtained by microarray hybridization from the database of the US National Cancer Institute with the 50% growth inhibition concentration values for eight ARSs (ARS, arteether (ARE), artesunate (ART), artemisetene, arteanuine B, dihydroartemisinylester stereoisomers 1 and 2). The constitutive expression of 30 genes correlated significantly with the cellular response to ARSs. By means of hierarchical cluster analysis and cluster image mapping expression, profiles were identified that determined significantly the cellular response to ART, ARE, artemether and dihydroartemisinylester stereoisomer 1. We have exemplarily validated the microarray data of six out of these 30 genes by realtime RT-PCR in seven cell lines. The fact that sensitivity and resistance of tumor cells could be predicted by the mRNA expression of angiogenesisrelated genes indicate that ARSs reveal their antitumor effects at least in part by inhibition of tumor angiogenesis. As many chemopreventive drugs exert antiangiogenic features, ARSs might also be chemopreventive in addition to their cytotoxic effects.

show abstract

“…Delphinidin inhibited cell migration [150], as well as hydrolyzable tannins, which also inhibited MMP-2 and -9 activities without suppressing the activation of ERK-MAPK or PI3K/AKT pathways [157]. EGCG prevented metastasis and invasion through its inhibitory effects on expression or activity of MMP [143,144,158,159] and focal adhesion kinase (FAK) and without affecting MT1-MMP and tissue inhibitor of MMP-2 (TIMP-2) [158,159]. Similarly, green tea catechins such as EGCG, catechin-gallate and ECG inhibited in a time-and dose-dependent manner MMP-9 secretion and mRNA stabilizing factor HuR, which plays a pivotal role in the development of tumours, whereas the 67 kDa laminin remained unaffected [160].…”

Section: Inhibition Of Metastasismentioning

confidence: 99%

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Ramos¹

2008

Molecular Nutrition Food Res

627

499

View full text Add to dashboard Cite

Prevention of cancer through dietary intervention recently has received an increasing interest, and dietary polyphenols have become not only important potential chemopreventive, but also therapeutic, natural agents. Polyphenols have been reported to interfere at the initiation, promotion and progression of cancer. They might lead to the modulation of proteins in diverse pathways and require the integration of different signals for the final chemopreventive or therapeutic effect. Polyphenols have been demonstrated to act on multiple key elements in signal transduction pathways related to cellular proliferation, differentiation, apoptosis, inflammation, angiogenesis and metastasis; however, these molecular mechanisms of action are not completely characterized and many features remain to be elucidated. The aim of this review is to provide insights into the molecular basis of potential chemopreventive and therapeutic activities of dietary polyphenols with emphasis in their ability to control intracellular signalling cascades considered as relevant targets in a cancer preventive approach.

show abstract

(−)-Epigallocatechin gallate inhibits membrane-type 1 matrix metalloproteinase, MT1-MMP, and tumor angiogenesis

Cited by 76 publications

References 17 publications

Purinergic regulation of angiogenesis by human breast carcinoma-secreted nucleoside diphosphate kinase

Purinergic regulation of angiogenesis by human breast carcinoma-secreted nucleoside diphosphate kinase

Microarray expression profiles of angiogenesis-related genes predict tumor cell response to artemisinins

Cancer chemoprevention and chemotherapy: Dietary polyphenols and signalling pathways

Contact Info

Product

Resources

About