Anticancer research · 2025
The Polyphenol (-)-Epigallocatechin-3-gallate (EGCG) Inhibits the Proliferation of Gastric Cancer Cells and Alters microRNA Signatures.
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Sasaki Kota, Fujita Koji, Fujihara Shintaro, Iwama Hisakazu, Kitaoka Atsuo, Suetsugu Fumiyuki, Mimura Shima, Tani Joji, Morishita Asahiro, Masaki Tsutomu, Kobara Hideki
Аннотация
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 in vitro and in vivo 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.
MATERIALS AND METHODS: 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.
RESULTS: 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 (p =0.000175), whereas hsa-miR-5787 was significantly down-regulated (p=0.000054).
CONCLUSION: Variable miRNAs were identified as promising therapeutic targets, with the potential to enhance the efficacy of EGCG in the treatment of gastric cancer.
MATERIALS AND METHODS: 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.
RESULTS: 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 (p =0.000175), whereas hsa-miR-5787 was significantly down-regulated (p=0.000054).
CONCLUSION: Variable miRNAs were identified as promising therapeutic targets, with the potential to enhance the efficacy of EGCG in the treatment of gastric cancer.