Jaceosidin induces apoptosis and inhibits migration in AGS gastric cancer cells by regulating ROS-mediated signaling pathways.

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Redox Report Pub Date : 2024-12-01 Epub Date: 2024-02-06 DOI:10.1080/13510002.2024.2313366
Jian Liu, Shu-Mei Li, Yan-Jun Tang, Jing-Long Cao, Wen-Shuang Hou, An-Qi Wang, Chang Wang, Cheng-Hao Jin
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Abstract

Jaceosidin (JAC) is a natural flavonoid with anti-oxidant and other pharmacological activities; however, its anti-cancer mechanism remains unclear. We investigated the mechanism of action of JAC in gastric cancer cells. Cytotoxicity and apoptosis assays showed that JAC effectively killed multiple gastric cancer cells and induced apoptosis in human gastric adenocarcinoma AGS cells via the mitochondrial pathway. Network pharmacological analysis suggested that its activity was linked to reactive oxygen species (ROS), AKT, and MAPK signaling pathways. Furthermore, JAC accumulated ROS to up-regulate p-JNK, p-p38, and IκB-α protein expressions and down-regulate the p-ERK, p-STAT3, and NF-κB protein expressions. Cell cycle assay results showed that JAC accumulated ROS to up-regulate p21 and p27 protein expressions and down-regulate p-AKT, CDK2, CDK4, CDK6, Cyclin D1, and Cyclin E protein expressions to induce G0/G1 phase arrest. Cell migration assay results showed JAC accumulated ROS to down-regulate Wnt-3a, p-GSK-3β, N-cadherin, and β-catenin protein expressions and up-regulate E-cadherin protein expression to inhibit migration. Furthermore, N-acetyl cysteine pre-treatment prevented the change of these protein expressions. In summary, JAC induced apoptosis and G0/G1 phase arrest and inhibited migration through ROS-mediated signaling pathways in AGS cells.

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栀子苷通过调节 ROS 介导的信号通路诱导 AGS 胃癌细胞凋亡并抑制其迁移。
Jaceosidin(JAC)是一种天然类黄酮,具有抗氧化和其他药理活性,但其抗癌机制仍不清楚。我们研究了 JAC 对胃癌细胞的作用机制。细胞毒性和细胞凋亡试验表明,江淮异黄酮能有效杀死多种胃癌细胞,并通过线粒体途径诱导人胃腺癌 AGS 细胞凋亡。网络药理学分析表明,其活性与活性氧(ROS)、AKT 和 MAPK 信号通路有关。此外,JAC 积累的 ROS 能上调 p-JNK、p-p38 和 IκB-α 蛋白表达,下调 p-ERK、p-STAT3 和 NF-κB 蛋白表达。细胞周期检测结果表明,JAC 可积累 ROS,上调 p21 和 p27 蛋白表达,下调 p-AKT、CDK2、CDK4、CDK6、Cyclin D1 和 Cyclin E 蛋白表达,诱导 G0/G1 期停滞。细胞迁移试验结果表明,JAC 积累的 ROS 可下调 Wnt-3a、p-GSK-3β、N-cadherin 和 β-catenin 蛋白表达,上调 E-cadherin 蛋白表达,从而抑制细胞迁移。此外,N-乙酰半胱氨酸预处理可阻止这些蛋白表达的变化。总之,JAC通过ROS介导的信号通路诱导AGS细胞凋亡和G0/G1期停滞,并抑制其迁移。
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来源期刊
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
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