Wang Min, Lei Yi-Xiong
School of Public Health, Guangzhou Medical University Guangzhou 510182, People's Republic of China.
Int J Clin Exp Med. 2015 Feb 15;8(2):3054-62. eCollection 2015.
To investigate the roles and mechanism(s) of epigallocatechin gallate (EGCG) in carcinogenesis in malignant transformed cell line, cadmium-induced malignant transformed cells were treated with different doses of EGCG. Then cell proliferation, cell apoptosis, hTERT mRNA and protein level, and c-Myc protein levels were measured at different time points. EGCG was found to inhibit cell proliferation in a dose-dependent manner. Cell cycle was changed in the transformed cells after EGCG treatment with significantly increased cell numbers in G0/G1 phase and decreased cell numbers in S phase compared to control group, P < 0.001. EGCG was also found to promote cell apoptosis with a time-dependent manner. Both mRNA and protein levels of hTERT gene were significantly decreased in cells after treated with EGCG, P < 0.001. c-Myc protein level was significantly decreased after EGCG treatment, especially in the highest dose group (i.e. 200 μg/ml). The decrease in c-Myc protein level was accompanied by the reduction of hTERT protein levels. EGCG can inhibit cell proliferation and promote apoptosis in malignant cadmium-transformed cell line. The mechanism may be its ability to reduce c-Myc gene expression and consequently inhibits hTERT gene expression, which in turn decrease the telomerase activity.
为研究表没食子儿茶素没食子酸酯(EGCG)在恶性转化细胞系致癌过程中的作用及机制,用不同剂量的EGCG处理镉诱导的恶性转化细胞。然后在不同时间点检测细胞增殖、细胞凋亡、hTERT mRNA和蛋白水平以及c-Myc蛋白水平。发现EGCG以剂量依赖性方式抑制细胞增殖。与对照组相比,EGCG处理后转化细胞的细胞周期发生改变,G0/G1期细胞数量显著增加,S期细胞数量减少,P<0.001。还发现EGCG以时间依赖性方式促进细胞凋亡。用EGCG处理后的细胞中,hTERT基因的mRNA和蛋白水平均显著降低,P<0.001。EGCG处理后c-Myc蛋白水平显著降低,尤其是在最高剂量组(即200μg/ml)。c-Myc蛋白水平的降低伴随着hTERT蛋白水平的降低。EGCG可抑制镉诱导的恶性转化细胞系的细胞增殖并促进其凋亡。其机制可能是EGCG能够降低c-Myc基因表达,进而抑制hTERT基因表达,从而降低端粒酶活性。