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
Chonnam University Research Institute of Medical Sciences, Chonnam University Medical School, Kwangju, Korea 501-190.
Br J Cancer. 2001 Mar 23;84(6):844-50. doi: 10.1054/bjoc.2000.1691.
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.
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。