Yamada Shuhei, Tsukamoto Shuntaro, Huang Yuhui, Makio Akiko, Kumazoe Motofumi, Yamashita Shuya, Tachibana Hirofumi
Division of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, Fukuoka 812-8581, Japan.
Sci Rep. 2016 Jan 12;6:19225. doi: 10.1038/srep19225.
MicroRNAs (miRNAs) are non-coding RNAs involved in various biological processes by regulating their target genes. Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) inhibits melanoma tumor growth by activating 67-kDa laminin receptor (67LR) signaling. To examine the effect of EGCG on miRNA expression in melanoma cells, we performed miRNA microarray analysis. We showed that EGCG up-regulated miRNA-let-7b expression through 67LR in melanoma cells. The EGCG-induced up-regulation of let-7b led to down-regulation of high mobility group A2 (HMGA2), a target gene related to tumor progression. 67LR-dependent cAMP/protein kinase A (PKA)/protein phosphatase 2A (PP2A) signaling pathway activation was involved in the up-regulation of let-7b expression induced by EGCG. These findings provide a basis for understanding the mechanism of miRNA regulation by EGCG.
微小RNA（miRNA）是一类非编码RNA，通过调控其靶基因参与多种生物学过程。绿茶多酚（-）-表没食子儿茶素-3-没食子酸酯（EGCG）通过激活67-kDa层粘连蛋白受体（67LR）信号通路抑制黑色素瘤肿瘤生长。为了研究EGCG对黑色素瘤细胞中miRNA表达的影响，我们进行了miRNA微阵列分析。我们发现EGCG通过67LR在黑色素瘤细胞中上调miRNA-let-7b的表达。EGCG诱导的let-7b上调导致与肿瘤进展相关的靶基因高迁移率族蛋白A2（HMGA2）的下调。67LR依赖的环磷酸腺苷/蛋白激酶A（PKA）/蛋白磷酸酶2A（PP2A）信号通路激活参与了EGCG诱导的let-7b表达上调。这些发现为理解EGCG对miRNA的调控机制提供了依据。
