1-Deoxynojirimycin Derivative Containing Tegafur Induced HCT-116 Cell Apoptosis through Mitochondrial Dysfunction and Oxidative Stress Pathway
文献类型： 外文期刊
作者： Tang, Liqing 1 ; Xu, Yixing 1 ; He, Jianglong 1 ; Huang, Gaiqun 2 ; Jiang, Xueping 1 ; Li, Yuqi 1 ; Li, Hao 1 ; Zhang, Ran 1 ; Gui, Zhongzheng 1 ;
作者机构： 1.Jiangsu Univ Sci & Technol, Sch Biotechnol, Zhenjiang 212100, Jiangsu, Peoples R China
2.Sichuan Acad Agr Sci, Sericultural Res Inst, Nanchong 637000, Sichuan, Peoples R China
3.Chinese Acad Agr Sci, Sericultural Res Inst, Zhenjiang 212100, Jiangsu, Peoples R China
关键词： 1-deoxynojirimycin; cell apoptosis; DNA damage; mitochondrial dysfunction; oxidative stress
期刊名称：ACS MEDICINAL CHEMISTRY LETTERS （ 影响因子：4.0； 五年影响因子：4.0 ）
ISSN： 1948-5875
年卷期： 2024 年 15 卷 11 期
页码：
收录情况： SCI
摘要： Three 1-deoxynojirimycin (DNJ) derivatives (named C4-C6) including DNJ and tegafur (TGF) were designed and synthesized, and their antiproliferative effects were investigated. C4-C6, especially C6, exerted good lipophilicity, alpha-glucosidase inhibitory activity, and antitumor effects. Mechanism studies indicated that C6 significantly induced cell apoptosis and S-phase block and inhibited migration of HCT-116 cells. Besides, C6 induced mitochondrial damage by decreasing the mitochondrial membrane potential, improving the accumulation of ROS, upregulating the expression of Bax, and downregulating Bcl-2. Moreover, C6 induced excessive production of ROS to trigger oxidative stress, resulting in an increase in the level of MDA and NO, a decrease in the content of GSH and SOD, and an overexpression of Nrf2. Furthermore, C6 induced DNA damage by down-regulating the expression of thymidylate synthase. These results indicated that C6 is a potential antitumor agent and kills HCT-116 cells through DNA damage, mitochondrial dysfunction, and oxidative stress.
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