Inaba Hiroyuki, Nagaoka Yasuo, Kushima Yukihiro, Kumagai Ayako, Matsumoto Yoshinori, Sakaguchi Minoru, Baba Kimiye, Uesato Shinichi
Department of Life Science and Biotechnology, Faculty of Chemistry, Material and Bioengineering, Kansai University, Suita, Osaka 564-8680, Japan.
Biol Pharm Bull. 2008 Jan;31(1):79-84. doi: 10.1248/bpb.31.79.
We compared anti-proliferative activities of (-)-epigallocatechin gallate (EGCG) and (-)-epigallocatechin (EGC) against HCT116 colorectal carcinoma cells. These catechins inhibited cell growth to nearly the same extent at low cell confluency in plates. However, their inhibitory effect grew weaker as cell confluence increased, and this tendency was more conspicuous for EGC than for EGCG. Both EGCG and EGC activated the phosphorylation of the major MAPKs, ERK, JNK, and p38, in the HCT116 cells as in many other established human cancer cells though to different extents. Cell cycle analyses, DNA fragmentation assays, and TUNEL assays as well as Western blot assays suggested that these catechins inhibited cell growth through mitogen-activated protein kinase (MAPK)-mediated apoptosis rather than cell cycle regulation.
我们比较了（-）-表没食子儿茶素没食子酸酯（EGCG）和（-）-表没食子儿茶素（EGC）对HCT116结肠癌细胞的抗增殖活性。在平板中细胞汇合度较低时，这些儿茶素对细胞生长的抑制程度几乎相同。然而，随着细胞汇合度增加，它们的抑制作用减弱，并且这种趋势在EGC中比在EGCG中更明显。与许多其他已建立的人类癌细胞一样，EGCG和EGC均能在不同程度上激活HCT116细胞中主要丝裂原活化蛋白激酶（MAPK）即细胞外调节蛋白激酶（ERK）、应激活化蛋白激酶（JNK）和p38的磷酸化。细胞周期分析、DNA片段化检测、末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）检测以及蛋白质免疫印迹分析表明，这些儿茶素通过丝裂原活化蛋白激酶（MAPK）介导的凋亡而非细胞周期调节来抑制细胞生长。
