Jo Eun-Hye, Lee Soo-Jin, Ahn Nam-Shik, Park Joon-Suk, Hwang Jae-Woong, Kim Sung-Hoon, Aruoma Okezie I, Lee Yong-Soon, Kang Kyung-Sun
Laboratory of Stem Cell and Tumor Biology, Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University, Seoul, Korea.
Eur J Cancer Prev. 2007 Aug;16(4):342-7. doi: 10.1097/01.cej.0000236247.86360.db.
Oligonol is a novel catechin-rich biotechnology product. The role of oligonol in modulating intracellular signaling mechanisms was investigated with the view of demonstrating its potential chemopreventive effect and the ability to inhibit cell proliferation using the estrogen-responsive MCF-7 and the estrogen-unresponsive MDA-MB-231 human breast cancer cell lines. Cell survival assay indicated that Oligonol was cytotoxic to both cells. Oligonol triggered apoptosis as revealed by the morphological features typical of nucleus staining and the accumulation of sub-G1 peak. Treatment with 25 microg/ml Oligonol resulted in an activation of caspase-7 and up-regulation of Bad on MCF-7 cells, while the Oligonol (20 microg/ml) induced up-regulation of Bcl-2 protein in a time-response manner on MDA-MB-231 cells. ERK1/2 in both cells were inactivated after Oligonol treatment in a time-dependent manner, and also inactivated upstream MEK1/2. Oligonol triggers apoptosis in MCF-7 and MDA-MB-231 cells through the modulation of pro-apoptotic Bcl-2 family proteins and MEK/ERK signaling pathway.
低聚原花青素是一种新型的富含儿茶素的生物技术产品。为了证明其潜在的化学预防作用以及使用雌激素反应性MCF-7和雌激素非反应性MDA-MB-231人乳腺癌细胞系抑制细胞增殖的能力，研究了低聚原花青素在调节细胞内信号传导机制中的作用。细胞存活分析表明，低聚原花青素对两种细胞均具有细胞毒性。如典型的细胞核染色形态特征和亚G1峰的积累所示，低聚原花青素引发了细胞凋亡。用25微克/毫升低聚原花青素处理导致MCF-7细胞中caspase-7的激活和Bad的上调，而低聚原花青素（20微克/毫升）在MDA-MB-231细胞上以时间响应方式诱导Bcl-2蛋白的上调。低聚原花青素处理后，两种细胞中的ERK1/2均以时间依赖性方式失活，并且上游的MEK1/2也失活。低聚原花青素通过调节促凋亡Bcl-2家族蛋白和MEK/ERK信号通路，在MCF-7和MDA-MB-231细胞中引发细胞凋亡。
