Department of Surgery, Cheng-Ching Hospital, Chung-Kang Branch, No. 118, Section 3, Chung Kang Road, Taichung City 40764, Taiwan.
Evid Based Complement Alternat Med. 2013;2013:306705. doi: 10.1155/2013/306705. Epub 2013 Jun 16.
Ellagic acid (EA) is able to inhibit the growth of several cancer cells; however, its effect on human ovarian carcinoma cells has not yet been investigated. Ovarian carcinoma ES-2 and PA-1 cells were treated with EA (10~100 μ M) and assessed for viability, cell cycle, apoptosis, anoikis, autophagy, and chemosensitivity to doxorubicin and their molecular mechanisms. EA inhibited cell proliferation in a dose- and time-dependent manner by arresting both cell lines at the G1 phase of the cell cycle, which were from elevating p53 and Cip1/p21 and decreasing cyclin D1 and E levels. EA also induced caspase-3-mediated apoptosis by increasing the Bax : Bcl-2 ratio and restored anoikis in both cell lines. The enhancement of apoptosis and/or inhibition of autophagy in these cells by EA assisted the chemotherapy efficacy. The results indicated that EA is a potential novel chemoprevention and treatment assistant agent for human ovarian carcinoma.
鞣花酸（EA）能够抑制多种癌细胞的生长；然而，其对人卵巢癌细胞的影响尚未得到研究。用人卵巢癌细胞 ES-2 和 PA-1 细胞处理 EA（10~100 μM），并评估其活力、细胞周期、细胞凋亡、失巢凋亡、自噬以及对阿霉素的化疗敏感性及其分子机制。EA 通过将两种细胞系阻滞在细胞周期的 G1 期，以剂量和时间依赖的方式抑制细胞增殖，这是通过升高 p53 和 Cip1/p21 并降低细胞周期蛋白 D1 和 E 水平实现的。EA 还通过增加 Bax:Bcl-2 比值诱导 caspase-3 介导的细胞凋亡，并恢复两种细胞系中的失巢凋亡。EA 增强这些细胞中的细胞凋亡和/或抑制自噬有助于化疗效果。结果表明，EA 是一种潜在的新型人卵巢癌化学预防和治疗辅助剂。
