Chen Z P, Schell J B, Ho C T, Chen K Y
Department of Chemistry, Rutgers, The State University of New Jersey, Piscataway 08855-0939, USA.
Cancer Lett. 1998 Jul 17;129(2):173-9. doi: 10.1016/s0304-3835(98)00108-6.
(-)-Epigallocatechin gallate (EGCG), a catechin polyphenol compound, represents the main ingredient of green tea extract. Although EGCG has been shown to be growth inhibitory in a number of tumor cell lines, it is not clear whether the effect is cancer-specific. In this study we compared the effect of EGCG on the growth of SV40 virally transformed WI38 human fibroblasts (WI38VA) with that of normal WI38 cells. The IC50 value of EGCG was estimated to be 120 and 10 microM for WI38 and WI38VA cells, respectively. Thus, EGCG at 40 microM completely inhibited the growth of WI38VA cells, but had little or no inhibitory effect on the growth of WI38 cells. Similar differential growth inhibition was also observed between a human colorectal cancer cell line (Caco-2), a breast cancer cell line (Hs578T) and their respective normal counterparts. EGCG at a concentration range of 40-200 microM induced a significant amount of apoptosis in WI38VA cultures, but not in WI38 cultures, as determined by terminal deoxynucleotidyl transferase assay. After exposure to EGCG at 200 microM for 8 h, more than 50% of WI38VA cells in a confluent culture became apoptotic. In contrast, less than 1% of WI38 cells displayed apoptotic labeling under the same condition. EGCG did not affect the serum-induced expression of c-fos and c-myc genes in normal WI38 cells. However, it significantly enhanced their expression in transformed W138VA cells. It is possible that differential modulation of certain genes, such as c-fos and c-myc, may cause differential effects of EGCG on the growth and death of cancer cells.
(-)-表没食子儿茶素没食子酸酯(EGCG)是一种儿茶素多酚化合物,是绿茶提取物的主要成分。尽管EGCG已被证明在多种肿瘤细胞系中具有生长抑制作用,但尚不清楚这种作用是否具有癌症特异性。在本研究中,我们比较了EGCG对SV40病毒转化的WI38人成纤维细胞(WI38VA)和正常WI38细胞生长的影响。EGCG对WI38和WI38VA细胞的IC50值分别估计为120和10微摩尔。因此,40微摩尔的EGCG完全抑制了WI38VA细胞的生长,但对WI38细胞的生长几乎没有抑制作用。在人结肠癌细胞系(Caco-2)、乳腺癌细胞系(Hs578T)及其各自的正常对应物之间也观察到了类似的差异生长抑制。通过末端脱氧核苷酸转移酶测定法确定,浓度范围为40-200微摩尔的EGCG在WI38VA培养物中诱导了大量细胞凋亡,但在WI38培养物中没有。在200微摩尔的EGCG中暴露8小时后,汇合培养物中超过50%的WI38VA细胞发生凋亡。相比之下,在相同条件下,不到1%的WI38细胞显示出凋亡标记。EGCG不影响正常WI38细胞中血清诱导的c-fos和c-myc基因的表达。然而,它显著增强了它们在转化的W138VA细胞中的表达。某些基因(如c-fos和c-myc)的差异调节可能导致EGCG对癌细胞生长和死亡产生不同的影响。