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1
EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells.表没食子儿茶素没食子酸酯(EGCG)是绿茶的主要成分,它通过抑制人结肠癌细胞中的血管内皮生长因子(VEGF)诱导来抑制肿瘤生长。
Br J Cancer. 2001 Mar 23;84(6):844-50. doi: 10.1054/bjoc.2000.1691.
2
The green tea compound, (-)-epigallocatechin-3-gallate downregulates N-cadherin and suppresses migration of bladder carcinoma cells.绿茶成分(-)-表没食子儿茶素-3-没食子酸酯可下调N-钙黏蛋白并抑制膀胱癌细胞的迁移。
J Cell Biochem. 2007 Oct 1;102(2):377-88. doi: 10.1002/jcb.21299.
3
(-)-Epigallocatechin gallate inhibits growth and activation of the VEGF/VEGFR axis in human colorectal cancer cells.(-)-表没食子儿茶素没食子酸酯抑制人结直肠癌细胞中 VEGF/VEGFR 轴的生长和激活。
Chem Biol Interact. 2010 May 14;185(3):247-52. doi: 10.1016/j.cbi.2010.03.036. Epub 2010 Mar 25.
4
Epigallocatechin-3-gallate-induced stress signals in HT-29 human colon adenocarcinoma cells.表没食子儿茶素-3-没食子酸酯在HT-29人结肠腺癌细胞中诱导应激信号。
Carcinogenesis. 2003 Aug;24(8):1369-78. doi: 10.1093/carcin/bgg091. Epub 2003 Jun 19.
5
Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo.绿茶多酚及其成分表没食子儿茶素没食子酸酯在体外和体内均能抑制人乳腺癌细胞的增殖。
Cancer Lett. 2007 Jan 8;245(1-2):232-41. doi: 10.1016/j.canlet.2006.01.027. Epub 2006 Mar 6.
6
[Epigallocatechin-3-gallate inhibits growth and angiogenesis of gastric cancer and its molecular mechanism].表没食子儿茶素-3-没食子酸酯抑制胃癌生长和血管生成及其分子机制
Zhonghua Wei Chang Wai Ke Za Zhi. 2009 Jan;12(1):82-5.
7
Epigallocatechin-3-gallate inhibits the PDGF-induced VEGF expression in human vascular smooth muscle cells via blocking PDGF receptor and Erk-1/2.表没食子儿茶素-3-没食子酸酯通过阻断血小板衍生生长因子(PDGF)受体和细胞外信号调节激酶1/2(Erk-1/2)来抑制PDGF诱导的人血管平滑肌细胞中血管内皮生长因子(VEGF)的表达。
Int J Oncol. 2006 Nov;29(5):1247-52.
8
(-)-Epigallocatechin-3-gallate promotes pro-matrix metalloproteinase-7 production via activation of the JNK1/2 pathway in HT-29 human colorectal cancer cells.(-)-表没食子儿茶素-3-没食子酸酯通过激活HT-29人结肠癌细胞中的JNK1/2途径促进基质金属蛋白酶-7前体的产生。
Carcinogenesis. 2005 Sep;26(9):1553-62. doi: 10.1093/carcin/bgi104. Epub 2005 Apr 28.
9
Mechanisms of inhibition of tumor angiogenesis and vascular tumor growth by epigallocatechin-3-gallate.表没食子儿茶素-3-没食子酸酯抑制肿瘤血管生成和血管性肿瘤生长的机制
Clin Cancer Res. 2004 Jul 15;10(14):4865-73. doi: 10.1158/1078-0432.CCR-03-0672.
10
Green tea catechins augment the antitumor activity of doxorubicin in an in vivo mouse model for chemoresistant liver cancer.绿茶儿茶素增强了多柔比星在体内耐药肝癌小鼠模型中的抗肿瘤活性。
Int J Oncol. 2010 Jul;37(1):111-23.

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1
The Therapeutic Potential of EGCG and Pro-EGCG in Mitigating Ovarian Hyperstimulation Syndrome: Unraveling the Modulatory Mechanism through the VEGF Pathway.表没食子儿茶素没食子酸酯(EGCG)和原表没食子儿茶素(Pro-EGCG)在减轻卵巢过度刺激综合征中的治疗潜力:通过血管内皮生长因子(VEGF)途径阐明调节机制
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Cancers (Basel). 2025 Feb 13;17(4):623. doi: 10.3390/cancers17040623.
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Chemoprophylaxis Effect of EGCG on the Recurrence of Colorectal Cancer: A Systematic Review and Meta-Analysis.EGCG 对结直肠癌复发的化学预防作用:系统评价和荟萃分析。
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Curr Pharm Biotechnol. 2024;25(5):599-622. doi: 10.2174/0113892010242028231002075512.
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Association of tea and its extracts with colorectal adenomas: meta-analysis and systematic review.茶及其提取物与结直肠腺瘤的关联:荟萃分析与系统评价
Front Nutr. 2023 Oct 5;10:1241848. doi: 10.3389/fnut.2023.1241848. eCollection 2023.
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Epigallocatechin-3-Gallate, an Active Green Tea Component to Support Anti-VEGFA Therapy in Wet Age-Related Macular Degeneration.没食子酸表没食子儿茶素酯,一种支持湿性年龄相关性黄斑变性抗 VEGF 治疗的绿茶有效成分。
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The Labyrinthine Landscape of APP Processing: State of the Art and Possible Novel Soluble APP-Related Molecular Players in Traumatic Brain Injury and Neurodegeneration.淀粉样前体蛋白(APP)加工的错综复杂景观:创伤性脑损伤和神经退行性变中最新的可溶性 APP 相关分子的可能新靶点。
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本文引用的文献

1
Extracellular signal-regulated kinase activation is required for up-regulation of vascular endothelial growth factor by serum starvation in human colon carcinoma cells.在人结肠癌细胞中,血清饥饿上调血管内皮生长因子需要细胞外信号调节激酶激活。
Cancer Res. 1999 Oct 1;59(19):4804-7.
2
Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo.丝裂原活化蛋白激酶(MAP)信号通路的阻断可抑制体内结肠肿瘤的生长。
Nat Med. 1999 Jul;5(7):810-6. doi: 10.1038/10533.
3
Angiostatic activity of synthetic inhibitors of urokinase type plasminogen activator.尿激酶型纤溶酶原激活剂合成抑制剂的血管生成抑制活性
Oncol Rep. 1999 May-Jun;6(3):523-6. doi: 10.3892/or.6.3.523.
4
Angiogenesis inhibited by drinking tea.喝茶可抑制血管生成。
Nature. 1999 Apr 1;398(6726):381. doi: 10.1038/18793.
5
Epigallocathechin-3 gallate selectively inhibits the PDGF-BB-induced intracellular signaling transduction pathway in vascular smooth muscle cells and inhibits transformation of sis-transfected NIH 3T3 fibroblasts and human glioblastoma cells (A172).表没食子儿茶素-3-没食子酸酯选择性抑制血小板衍生生长因子-BB(PDGF-BB)诱导的血管平滑肌细胞内信号转导通路,并抑制转染sis的NIH 3T3成纤维细胞和人胶质母细胞瘤细胞(A172)的转化。
Mol Biol Cell. 1999 Apr;10(4):1093-104. doi: 10.1091/mbc.10.4.1093.
6
Induction of apoptosis in prostate cancer cell lines by the green tea component, (-)-epigallocatechin-3-gallate.绿茶成分(-)-表没食子儿茶素-3-没食子酸酯对前列腺癌细胞系凋亡的诱导作用
Cancer Lett. 1998 Aug 14;130(1-2):1-7. doi: 10.1016/s0304-3835(98)00084-6.
7
Regulation of vascular endothelial growth factor expression in human colon cancer by insulin-like growth factor-I.胰岛素样生长因子-I对人结肠癌中血管内皮生长因子表达的调控
Cancer Res. 1998 Sep 1;58(17):4008-14.
8
Black tea and mammary gland carcinogenesis by 7,12-dimethylbenz[a]anthracene in rats fed control or high fat diets.红茶与7,12-二甲基苯并[a]蒽在喂食对照或高脂饮食大鼠中诱发乳腺癌的关系
Carcinogenesis. 1998 Jul;19(7):1269-73. doi: 10.1093/carcin/19.7.1269.
9
Cancer inhibition by green tea.绿茶对癌症的抑制作用。
Mutat Res. 1998 Jun 18;402(1-2):307-10. doi: 10.1016/s0027-5107(97)00310-2.
10
p42/p44 MAP kinase module plays a key role in the transcriptional regulation of the vascular endothelial growth factor gene in fibroblasts.p42/p44丝裂原活化蛋白激酶模块在成纤维细胞中血管内皮生长因子基因的转录调控中起关键作用。
J Biol Chem. 1998 Jul 17;273(29):18165-72. doi: 10.1074/jbc.273.29.18165.

表没食子儿茶素没食子酸酯(EGCG)是绿茶的主要成分,它通过抑制人结肠癌细胞中的血管内皮生长因子(VEGF)诱导来抑制肿瘤生长。

EGCG, a major component of green tea, inhibits tumour growth by inhibiting VEGF induction in human colon carcinoma cells.

作者信息

Jung Y D, Kim M S, Shin B A, Chay K O, Ahn B W, Liu W, Bucana C D, Gallick G E, Ellis L M

机构信息

Chonnam University Research Institute of Medical Sciences, Chonnam University Medical School, Kwangju, Korea 501-190.

出版信息

Br J Cancer. 2001 Mar 23;84(6):844-50. doi: 10.1054/bjoc.2000.1691.

DOI:10.1054/bjoc.2000.1691
PMID:11259102
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2363808/
Abstract

Catechins are key components of teas that have antiproliferative properties. We investigated the effects of green tea catechins on intracellular signalling and VEGF induction in vitro in serum-deprived HT29 human colon cancer cells and in vivo on the growth of HT29 cells in nude mice. In the in vitro studies, (-)-epigallocatechin gallate (EGCG), the most abundant catechin in green tea extract, inhibited Erk-1 and Erk-2 activation in a dose-dependent manner. However, other tea catechins such as (-)-epigallocatechin (EGC), (-)-epicatechin gallate (ECG), and (-)-epicatechin (EC) did not affect Erk-1 or 2 activation at a concentration of 30 microM. EGCG also inhibited the increase of VEGF expression and promoter activity induced by serum starvation. In the in vivo studies, athymic BALB/c nude mice were inoculated subcutaneously with HT29 cells and treated with daily intraperitoneal injections of EC (negative control) or EGCG at 1.5 mg day(-1)mouse(-1)starting 2 days after tumour cell inoculation. Treatment with EGCG inhibited tumour growth (58%), microvessel density (30%), and tumour cell proliferation (27%) and increased tumour cell apoptosis (1.9-fold) and endothelial cell apoptosis (3-fold) relative to the control condition (P< 0.05 for all comparisons). EGCG may exert at least part of its anticancer effect by inhibiting angiogenesis through blocking the induction of VEGF.

摘要

儿茶素是茶叶中具有抗增殖特性的关键成分。我们研究了绿茶儿茶素对血清饥饿的HT29人结肠癌细胞体外细胞内信号传导和VEGF诱导的影响,以及对裸鼠体内HT29细胞生长的影响。在体外研究中,绿茶提取物中含量最丰富的儿茶素(-)-表没食子儿茶素没食子酸酯(EGCG)以剂量依赖性方式抑制Erk-1和Erk-2的激活。然而,其他茶儿茶素,如(-)-表没食子儿茶素(EGC)、(-)-表儿茶素没食子酸酯(ECG)和(-)-表儿茶素(EC)在30 microM浓度下不影响Erk-1或2的激活。EGCG还抑制了血清饥饿诱导的VEGF表达增加和启动子活性。在体内研究中,无胸腺BALB/c裸鼠皮下接种HT29细胞,并在肿瘤细胞接种后2天开始每天腹腔注射EC(阴性对照)或1.5 mg·day⁻¹·mouse⁻¹的EGCG进行治疗。与对照条件相比,EGCG治疗抑制了肿瘤生长(58%)、微血管密度(30%)和肿瘤细胞增殖(27%),并增加了肿瘤细胞凋亡(1.9倍)和内皮细胞凋亡(3倍)(所有比较P<0.05)。EGCG可能至少部分通过阻断VEGF的诱导抑制血管生成来发挥其抗癌作用。