Umeda Daisuke, Tachibana Hirofumi, Yamada Koji
Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
Biochem Biophys Res Commun. 2005 Jul 29;333(2):628-35. doi: 10.1016/j.bbrc.2005.05.108.
Epigallocatechin-3-O-gallate (EGCG), a major polyphenol of green tea, has been shown to inhibit the growth of various cancer cell lines. We show here that EGCG induced the disruption of stress fibers and decreased the phosphorylation of the myosin II regulatory light chain (MRLC) at Thr18/Ser19, which is necessary for both contractile ring formation and cell division. Indirect immunofluorescence analysis revealed that EGCG inhibited the concentration of both F-actin and the phosphorylated MRLC in the cleavage furrow at the equator of dividing cells. In addition, EGCG increased the percentages of cells in the G(2)/M phase and inhibited cell growth. Recently, we have demonstrated that the anticancer activity of EGCG is mediated by the metastasis-associated 67kDa laminin receptor (67LR). To explore whether the effect of EGCG is mediated by the 67LR, we transfected cells with short hairpin RNA (shRNA) expression vector to downregulate 67LR expression. When the 67LR was silenced, the suppressive effect of EGCG on the MRLC phosphorylation was significantly attenuated. These results suggest that EGCG inhibits the cell growth by reducing the MRLC phosphorylation and this effect is mediated by the 67LR.
表没食子儿茶素-3-没食子酸酯（EGCG）是绿茶中的一种主要多酚，已被证明能抑制多种癌细胞系的生长。我们在此表明，EGCG诱导应力纤维的破坏，并降低肌球蛋白II调节轻链（MRLC）在苏氨酸18/丝氨酸19位点的磷酸化，这对于收缩环形成和细胞分裂都是必需的。间接免疫荧光分析显示，EGCG抑制分裂细胞赤道处分裂沟中F-肌动蛋白和磷酸化MRLC的聚集。此外，EGCG增加了处于G(2)/M期的细胞百分比并抑制细胞生长。最近，我们已经证明EGCG的抗癌活性是由转移相关的67kDa层粘连蛋白受体（67LR）介导的。为了探究EGCG的作用是否由67LR介导，我们用短发夹RNA（shRNA）表达载体转染细胞以下调67LR的表达。当67LR沉默时，EGCG对MRLC磷酸化的抑制作用明显减弱。这些结果表明，EGCG通过降低MRLC磷酸化来抑制细胞生长，并且这种作用是由67LR介导的。
