Epigallocatechin-3-gallate (EGCG), a major polyphenol component of green tea, presents anticancer efficacy. However, its exact mechanism of action is not known. In this study, we evaluated the effect of EGCG alone or in combination with current chemotherapeutics [gemcitabine, 5-flourouracil (5-FU), and doxorubicin] on pancreatic, colon, and lung cancer cell growth, as well as the mechanisms involved in the combined action. EGCG reduced pancreatic, colon, and lung cancer cell growth in a concentration and time-dependent manner. EGCG strongly induced apoptosis and blocked cell cycle progression. Moreover, EGCG enhanced the growth inhibitory effect of 5-FU and doxorubicin. Of note, EGCG enhanced 5-FU's and doxorubicin's effect on apoptosis, but not on cell cycle. Mechanistically, EGCG reduced ERK phosphorylation concentration-dependently, and sensitized gemcitabine, 5-FU, and doxorubicin to further suppress ERK phosphorylation in multiple cancer cell lines. In conclusion, EGCG presents a strong anticancer effect in pancreatic, colon, and lung cancer cells and is a robust combination partner for multiple chemotherapeutics as evidenced by reducing cancer cell growth, in part, by inhibiting the ERK pathway.

表没食子儿茶素-3-没食子酸酯 (EGCG) 是绿茶的主要多酚成分，具有抗癌功效。然而，其确切的作用机制尚不清楚。在本研究中，我们评估了 EGCG 单独或与当前化疗药物 [吉西他滨、5-氟尿嘧啶 (5-FU) 和多柔比星] 联合对胰腺、结肠和肺癌细胞生长的影响，以及参与的机制联合行动。EGCG 以浓度和时间依赖性方式减少胰腺、结肠和肺癌细胞的生长。EGCG 强烈诱导细胞凋亡并阻止细胞周期进程。此外，EGCG 增强了 5-FU 和阿霉素的生长抑制作用。值得注意的是，EGCG 增强了 5-FU 和阿霉素对细胞凋亡的影响，但对细胞周期没有影响。从机制上讲，EGCG 浓度依赖性地降低 ERK 磷酸化，并敏化吉西他滨、5-FU 和阿霉素，以进一步抑制多种癌细胞系中的 ERK 磷酸化。总之，EGCG 在胰腺癌细胞、结肠癌细胞和肺癌细胞中表现出强大的抗癌作用，并且是多种化疗药物的强大组合伙伴，这可以通过抑制 ERK 途径部分地减少癌细胞生长来证明。