Ding Ye, Li Hao, Cao Saisai, Yu Yong
Henan Key Laboratory of Helicobacter Pylori & Microbiota and Gastrointestinal Cancer, Marshall Medical Research Center, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China; Department of Gastroenterology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
Henan Key Laboratory of Helicobacter Pylori & Microbiota and Gastrointestinal Cancer, Marshall Medical Research Center, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China; Department of Gastroenterology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
Toxicol Appl Pharmacol. 2024 Sep;490:117036. doi: 10.1016/j.taap.2024.117036. Epub 2024 Jul 14.
Catechin is a kind of flavonoids, mainly derived from the plant Camellia sinensis. It has a strong antioxidant effect, and it also has significant therapeutic effects on anti-cancer, anti-diabetes, and anti-infection. This study was intended to look at how catechin affected the malignant biological activity of gastric cancer cells. We used databases to predict the targets of catechin and the pathogenic targets of gastric cancer. Venn diagram was used to find the intersection genes, the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were performed on intersection genes. Using the STRING database, the Protein-Protein Interaction (PPI) network was built. The top 8 genes were screened by Cytoscape 3.9.1, then their binding was verified by molecular docking. The proliferation ability, cell cycle, apoptosis and migration of gastric cancer cells were detected, as well as the protein expression levels of PI3K, p-AKT, and AKT and the mRNA expression levels of AKT1, VEGFA, EGFR, HRAS, and HSP90AA1 in gastric cancer cells. Our research revealed that different concentrations of catechin could effectively inhibit the proliferation and migration of gastric cancer cells, regulate the cell cycle, and promote the death of these cells, and it's possible that the PI3K/Akt pathway was crucial in mediating this impact. Moreover, adding the PI3K/Akt pathway agonist significantly reduced the promoting effect of catechin on the apoptosis of gastric cancer cells. This study suggested that catechin was a potential drug for the treatment of gastric cancer.
儿茶素是一种黄酮类化合物,主要来源于植物茶树。它具有很强的抗氧化作用,对抗癌、抗糖尿病和抗感染也有显著的治疗效果。本研究旨在探讨儿茶素如何影响胃癌细胞的恶性生物学活性。我们利用数据库预测儿茶素的靶点和胃癌的致病靶点。使用维恩图找到交集基因,对交集基因进行京都基因与基因组百科全书(KEGG)和基因本体论(GO)富集分析。利用STRING数据库构建蛋白质-蛋白质相互作用(PPI)网络。通过Cytoscape 3.9.1筛选出前8个基因,然后通过分子对接验证它们的结合。检测胃癌细胞的增殖能力、细胞周期、凋亡和迁移情况,以及胃癌细胞中PI3K、p-AKT和AKT的蛋白表达水平和AKT1、VEGFA、EGFR、HRAS和HSP90AA1的mRNA表达水平。我们的研究表明,不同浓度的儿茶素可以有效抑制胃癌细胞的增殖和迁移,调节细胞周期,并促进这些细胞的死亡,PI3K/Akt通路可能在介导这种影响中起关键作用。此外,添加PI3K/Akt通路激动剂显著降低了儿茶素对胃癌细胞凋亡的促进作用。本研究表明儿茶素是一种潜在的胃癌治疗药物。