Tea catechins inhibit angiogenesis in vitro, measured by human endothelial cell growth, migration and tube formation, through inhibition of VEGF receptor binding

Kondo, Takako; Ohta, Toshiro; Igura, Koichi; Hara, Yukihiko; Kaji, Koichi

doi:10.1016/s0304-3835(02)00007-1

Cited by 151 publications

(103 citation statements)

References 29 publications

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“…Using human umbilical vein endothelial cells (HUVEC) as a model system, several independent researches (Abou-Agag et al 2001;Kondo et al 2002;Sartippour et al 2002;Singh et al 2002) have shown the inhibition of angiogenesis by green tea catechins and substantiated the in vivo data that drinking tea suppresses angiogenesis (Cao and Cao 1999;Kao et al 2000). In this study, we also confirmed the sensitivity of endothelial cells to catechins.…”

Section: Introductionsupporting

confidence: 82%

“…Using HUVEC as a model system, several independent researches have shown the inhibition of angiogenesis by green tea catechins (Abou-Agag et al 2001; Kondo et al 2002;Sartippour et al 2002;Singh et al 2002). Reflecting multiple mechanisms of the effect possible for these polyphenols (see Discussion), their effects on the growth of HUVEC have been controversial and were variable depending on the experimental conditions.…”

Section: Differential Effect Of Catechins On Three Ratec Clones and Hmentioning

confidence: 99%

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Differential effect of green tea catechins on three endothelial cell clones isolated from rat adipose tissue and on human umbilical vein endothelial cells

et al. 2004

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By single colony isolation from the cells in stromal vascular fraction (SVF) dispersed from rat adipose tissues, we isolated three independent clones with different proliferation potential. All clones showed cobblestone-like morphology at the confluence and incorporated fluorescent Dil acetylated low density lipoprotein. When plated on Matrigel, they formed a capillary network-like structure. These rat adipose tissue endothelial cell (RATEC) clones showed higher expression of wnt2, wnt4, wnt5a, wnt5b, fzd1 and fzd5 whereas lower expression of cell cycle controlling genes such as CIP1, KIP1, KIP2, CDKN2A, CDKN2B, CDKN2C and CDKN2D compared to human umbilical vein endothelial cell (HUVEC). As reported for HUVEC, the growth of RATEC was inhibited by green tea catechins such as epigallocatechin, epicatechin gallate, epicatechin and epigallocatechin gallate but with higher sensitivity than HUVEC. The sensitivity of RATEC to catechins was higher for the cultures with low plating density and for the clone with higher proliferation potential.

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Section: Introductionsupporting

confidence: 82%

Section: Differential Effect Of Catechins On Three Ratec Clones and Hmentioning

confidence: 99%

Differential effect of green tea catechins on three endothelial cell clones isolated from rat adipose tissue and on human umbilical vein endothelial cells

et al. 2004

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“…25,[38][39][40][41] Importantly, our results demonstrate that EGCG can counter VEGF without downregulating VEGFR-2 expression levels.…”

Section: Discussionmentioning

confidence: 53%

“…EGCG may accomplish this by inhibiting the binding of VEGF to VEGF-R, 39 or by suppressing VEGF-R phosphorylation as previously reported. 25,29 However, it is unclear whether the latter is required for complex formation.…”

Section: Discussionmentioning

confidence: 63%

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Rodriguez

Guo

Liu

et al. 2005

Intl Journal of Cancer

116

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A potential mechanism by which green tea may prevent cancer development is through the inhibition of angiogenesis. We have shown previously that the green tea catechin, epigallocatechin gallate (EGCG), inhibits endothelial cell tube formation through the inhibition of vascular endothelial growth factor (VEGF)-induced Akt activation and vascular endothelial (VE)-cadherin phosphorylation. Furthermore, EGCG can suppress oxidant-induced production of the proangiogenic cytokine interleukin (IL)-8. To further elucidate the antiangiogenic mechanisms of EGCG, we investigated its regulation of other molecular processes in VEGFinduced signaling in human umbilical vein endothelial cells (HUVECs). We show that EGCG at physiological doses (0.5-10 lM) markedly inhibits the formation of a vascular endothelial growth factor receptor 2 complex formed upon the binding of its ligand VEGF. This disruption results in a significant and dosedependent decrease in PI3-kinase activity. Electrophoretic mobility shift assay revealed that EGCG decreased the PI3 kinasedependent activation and DNA-binding ability of NF-jB, likely acting through decreasing phosphorylation and degradation of IjB. VEGF-induced IL-8 production at the mRNA (real time RT-PCR) and protein levels (ELISA) are also suppressed with EGCG. These results suggest a novel mechanism for green tea's anticancer effects where EGCG can abrogate VEGF signaling by interfering with the formation of a receptor complex, resulting in attenuated mitogenic and angiogenic signaling. ' 2005 Wiley-Liss, Inc.

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“…Interestingly Li et al demonstrated that EGCG competitively binds to the ATP binding site of IGF-R1 inhibiting its kinase activity, in vitro (IC50 = 14 μmol/L) and in vivo [60]. The blockage of ligandreceptor binding has been suggested as the mechanism behind the inhibitory effect of GTCs, on PDGFR and HGFR in multiple cell lines, at concentrations of 1÷10 μM [58,[75][76][77]. Tachibana et al proposed that EGCG is a ligand of the 67-kDa laminin receptor (67-LR) with a dissociation constant (Kd) value of 0.004 μM [78].…”

Section: Cell Surface Receptorsmentioning

confidence: 99%

Green Tea Catechins for Prostate Cancer Prevention: Present Achievements and Future Challenges

Naponelli¹,

Ramazzina²,

Lenzi³

et al. 2017

Preprint

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Green Tea Catechins (GTCs) are a family of chemically related compounds usually classified as antioxidant molecules. Epidemiological evidences, supported by interventional studies, highlighted a more than promising role for GTCs in human Prostate Cancer (PCa) chemoprevention.In the last decades many efforts have been made to gain new insights into the mechanism of action of GTCs. Now it is clear that GTCs anticancer action can no longer be simplistically limited to their direct antioxidant/pro-oxidant properties. Recent contributions to the advancement of knowledge in this field have shown that GTCs specifically interact with cellular targets including, cell surface receptors, lipid rafts and endoplasmic reticulum, modulate gene expression through direct effect on transcription factors or indirect epigenetic mechanisms, interfere with intracellular proteostasis at various levels. Many of the effects observed in vitro are dose and cell context dependent and take place at concentration that cannot be achieved in vivo.Poor intestinal absorption together with an extensive systemic and enteric metabolism influence GTCs bioavailability through still poor understood mechanisms. Recent efforts to develop delivery systems that increase GTCs overall bioavailability, by mean of biopolymeric nanoparticles, represent the main way to translate preclinical results in a real clinical scenario for PCa chemoprevention.

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Tea catechins inhibit angiogenesis in vitro, measured by human endothelial cell growth, migration and tube formation, through inhibition of VEGF receptor binding

Cited by 151 publications

References 29 publications

Differential effect of green tea catechins on three endothelial cell clones isolated from rat adipose tissue and on human umbilical vein endothelial cells

Differential effect of green tea catechins on three endothelial cell clones isolated from rat adipose tissue and on human umbilical vein endothelial cells

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Green Tea Catechins for Prostate Cancer Prevention: Present Achievements and Future Challenges

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