Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Mol Med Rep. 2014 Mar;9(3):1085-9. doi: 10.3892/mmr.2014.1909. Epub 2014 Jan 22.
Epigallocatechin‑3‑gallate (EGCG), a major catechin in green tea, has recently been reported to exhibit anticancer effects on a number of types of cancer cells in vitro; however, the molecular mechanisms of this anticancer effect remain poorly understood. In the current study, the effects of EGCG on the proliferation and migration of the OVCAR‑3 human ovarian carcinoma cell line were investigated. Cells were treated with EGCG and their proliferation rates were determined by an MTT assay. In addition, cell migration was detected by transwell assay. The activity of mitogen‑activated protein kinases (MAPKs) and the expression of matrix metalloproteinase‑2/9 (MMP‑2/9) were examined by western blotting. The results showed that EGCG significantly inhibited (P<0.05) the proliferation of OVCAR‑3 cells in a time‑ and concentration‑dependent manner. EGCG (100 µM) time‑dependently increased (P<0.05) the activity of p38, but not extracellular signal‑regulated kinases 1/2. SB203580, a specific p38 MAPK inhibitor, completely diminished EGCG‑induced phosphorylation of p38 and partially blocked EGCG‑inhibited OVCAR‑3 cell proliferation. Furthermore, EGCG (0‑100 µM) dose‑dependently inhibited (P<0.05) OVCAR‑3 cell migration. The protein expression levels of MPP‑2, but not MMP‑9, were dose‑dependently decreased following treatment with EGCG (0‑100 µM) for 48 h. These data indicated that EGCG inhibited OVCAR‑3 cell proliferation and migration, potentially mediated via the activation of p38 MAPK and downregulation of the protein expression of MMP2. Thus, the therapeutic potential of EGCG for ovarian cancer requires further investigation.
没食子酸表没食子儿茶素酯（EGCG）是绿茶中的一种主要儿茶素，最近有报道称其在体外对多种类型的癌细胞具有抗癌作用；然而，这种抗癌作用的分子机制仍知之甚少。在本研究中，研究了 EGCG 对 OVCAR-3 人卵巢癌细胞系增殖和迁移的影响。用 EGCG 处理细胞，并通过 MTT 测定法测定细胞增殖率。此外，通过 Transwell 测定法检测细胞迁移。通过 Western blot 检测丝裂原激活蛋白激酶（MAPKs）的活性和基质金属蛋白酶-2/9（MMP-2/9）的表达。结果表明，EGCG 以时间和浓度依赖的方式显著抑制（P<0.05）OVCAR-3 细胞的增殖。EGCG（100 μM）时间依赖性地增加（P<0.05）p38 的活性，但不增加细胞外信号调节激酶 1/2 的活性。p38 MAPK 的特异性抑制剂 SB203580 完全消除了 EGCG 诱导的 p38 磷酸化，并部分阻断了 EGCG 抑制 OVCAR-3 细胞增殖的作用。此外，EGCG（0-100 μM）浓度依赖性地抑制（P<0.05）OVCAR-3 细胞迁移。用 EGCG（0-100 μM）处理 48 h 后，MMP-2 的蛋白表达水平呈剂量依赖性降低，但 MMP-9 的蛋白表达水平没有降低。这些数据表明，EGCG 抑制 OVCAR-3 细胞增殖和迁移，可能是通过激活 p38 MAPK 和下调 MMP2 的蛋白表达来介导的。因此，EGCG 治疗卵巢癌的潜力需要进一步研究。
