Yoo Hyeon G, Shin Boo A, Park Ju C, Kim Hong S, Kim Won J, Chay Kee O, Ahn Bong W, Park Rae K, Ellis Lee M, Jung Young D
Chonnam University Research Institute of Medical Sciences, Chonnam National University Medical School, Kwangju, Korea.
Anticancer Res. 2002 Nov-Dec;22(6A):3373-8.
We have previously shown that treatment with (-)-epigallocatechin-3-gallate (EGCG) inhibited vascularity and tumor growth in human colon cancer xenografts in nude mice (Jung et al: Br J Cancer 84, 2001). In this study, we examined whether endothelial cell death by EGCG is mediated by apoptosis and which molecular mechanisms are involved in this process. EGCG was found to suppress cell growth and induce apoptosis largely through mitochondrial depolarization, activation of caspase-3 and cleavage of DNA fragmentation factor-45 in human endothelial ECV 304 cells. The induction of apoptosis by EGCG was confirmed by cleaved and condensed nuclear chromatin and DNA hypoploidy. These results suggest that EGCG may exert at least part of its anticancer effect by inhibiting angiogenesis through inducing endothelial apoptosis.
我们之前已经表明，用（-）-表没食子儿茶素-3-没食子酸酯（EGCG）处理可抑制裸鼠人结肠癌异种移植物中的血管生成和肿瘤生长（Jung等人：《英国癌症杂志》84，2001年）。在本研究中，我们研究了EGCG引起的内皮细胞死亡是否由细胞凋亡介导，以及该过程涉及哪些分子机制。发现EGCG在人内皮ECV 304细胞中主要通过线粒体去极化、半胱天冬酶-3的激活和DNA片段化因子-45的裂解来抑制细胞生长并诱导细胞凋亡。通过裂解和浓缩的核染色质以及DNA亚二倍体证实了EGCG诱导的细胞凋亡。这些结果表明，EGCG可能通过诱导内皮细胞凋亡抑制血管生成，从而至少部分发挥其抗癌作用。
