Sasaki Kota, Fujita Koji, Fujihara Shintaro, Iwama Hisakazu, Kitaoka Atsuo, Suetsugu Fumiyuki, Mimura Shima, Tani Joji, Morishita Asahiro, Masaki Tsutomu, Kobara Hideki
Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan
Department of Gastroenterology and Neurology, Kagawa University, Kagawa, Japan.
Anticancer Res. 2025 Jul;45(7):2925-2936. doi: 10.21873/anticanres.17660.
BACKGROUND/AIM: The polyphenol (-)-epigallocatechin-3-gallate (EGCG), a primary catechin found in green tea, is known to inhibit cell proliferation and induce apoptosis in various cultured cells. However, its effect on gastric cancer cells and its effects on miRNA expression remain poorly understood. This study aimed to examine the effects of EGCG on gastric cancer cells and and analyze the expression profiles of microRNAs (miRNAs) in EGCG-treated gastric cancer cells, with the ultimate goal of elucidating the anticancer mechanisms of EGCG.
The inhibitory effect of EGCG on the growth of four gastric cancer cell lines (MKN-45, MKN-1, MKN-7, and MKN-74) was evaluated using a Cell Counting Kit-8 assay. A series of experiments was subsequently performed to investigate the effects of EGCG on MKN-45 cells, including cell cycle and apoptosis analyses, array analysis of phosphorylated receptor tyrosine kinases (RTKs) and angiogenic factors, and miRNA expression analyses. The antitumor effects of EGCG were also examined in a mouse xenograft model.
EGCG inhibited the proliferation of MKN-45 cells and induced apoptosis. Microarray analysis revealed changes in miRNA expression following EGCG treatment. Specifically, hsa-miR-5100 was significantly up-regulated ( =0.000175), whereas hsa-miR-5787 was significantly down-regulated (=0.000054).
Variable miRNAs were identified as promising therapeutic targets, with the potential to enhance the efficacy of EGCG in the treatment of gastric cancer.
背景/目的：表没食子儿茶素-3-没食子酸酯（EGCG）是绿茶中主要的儿茶素，已知其可抑制多种培养细胞的增殖并诱导凋亡。然而，其对胃癌细胞的作用以及对miRNA表达的影响仍知之甚少。本研究旨在探讨EGCG对胃癌细胞的影响，并分析EGCG处理的胃癌细胞中微小RNA（miRNA）的表达谱，最终目的是阐明EGCG的抗癌机制。
使用细胞计数试剂盒-8法评估EGCG对四种胃癌细胞系（MKN-45、MKN-1、MKN-7和MKN-74）生长的抑制作用。随后进行了一系列实验，以研究EGCG对MKN-45细胞的影响，包括细胞周期和凋亡分析、磷酸化受体酪氨酸激酶（RTK）和血管生成因子的阵列分析以及miRNA表达分析。还在小鼠异种移植模型中检测了EGCG的抗肿瘤作用。
EGCG抑制MKN-45细胞的增殖并诱导凋亡。微阵列分析显示EGCG处理后miRNA表达发生变化。具体而言，hsa-miR-5100显著上调（=0.000175），而hsa-miR-5787显著下调（=0.000054）。
可变miRNA被确定为有前景的治疗靶点，有可能增强EGCG治疗胃癌的疗效。
