School of Pharmacy and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, PR China; Natural Products Research Laboratories, UNC Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, NC, 27599, United States.
School of Pharmacy and Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, PR China.
Eur J Med Chem. 2018 Jun 25;154:199-209. doi: 10.1016/j.ejmech.2018.05.025. Epub 2018 May 18.
Fourteen novel amino-quinoline-5,8-dione derivatives (6a-h and 7a-h) were designed and synthesized by coupling different alkyl- or aryl-amino fragments at the C6- or C7-position of quinoline-5,8-dione. All target compounds showed antiproliferative potency in the low micromolar range in both drug sensitive HeLaS3 and multidrug resistant KB-vin cell lines. Compounds 6h, 6d, 7a, and 7d exhibited more potent antiproliferative effects than the other compounds. Especially, compounds 6d and 7d displayed NQO1-dependent cytotoxicity and competitive NQO1 inhibitory effects in both drug sensitive HeLaS3 and multidrug resistant KB-vin cell lines. Furthermore, compounds 6h, 6d, 7a, and 7d induced a dose-dependent lethal mitochondrial dysfunction in both drug sensitive HeLaS3 and multidrug resistant KB-vin cells by increasing intracellular reactive oxygen species (ROS) levels. Notably, compound 7d selectively inhibited cancer cells, but not non-tumor liver cell proliferation in vitro, and significantly triggered HeLaS3 cell apoptosis by regulating apoptotic proteins of Bcl-2, Bax, and cleaved caspase-3 in a dose-dependent manner. Our findings suggest that these novel C6- or C7-substituted amino-quinoline-5,8-dione derivatives, such as 7d, could be further developed in the future as potent and selective antitumor agents to potentially circumvent multi-drug resistance (MDR).
14 种新型的氨基-喹啉-5,8-二酮衍生物(6a-h 和 7a-h)通过在喹啉-5,8-二酮的 C6-或 C7-位连接不同的烷基-或芳基-氨基片段而设计和合成。所有目标化合物在低微摩尔范围内对药物敏感的 HeLaS3 和多药耐药的 KB-vin 细胞系均显示出抗增殖活性。化合物 6h、6d、7a 和 7d 比其他化合物表现出更强的抗增殖作用。特别是化合物 6d 和 7d 在药物敏感的 HeLaS3 和多药耐药的 KB-vin 细胞系中表现出 NQO1 依赖性细胞毒性和竞争性 NQO1 抑制作用。此外,化合物 6h、6d、7a 和 7d 通过增加细胞内活性氧(ROS)水平,在药物敏感的 HeLaS3 和多药耐药的 KB-vin 细胞中诱导剂量依赖性致死性线粒体功能障碍。值得注意的是,化合物 7d 选择性地抑制癌细胞,而不是非肿瘤肝细胞在体外增殖,并通过调节 Bcl-2、Bax 和 cleaved caspase-3 的凋亡蛋白,以剂量依赖的方式显著触发 HeLaS3 细胞凋亡。我们的研究结果表明,这些新型的 C6-或 C7-取代的氨基-喹啉-5,8-二酮衍生物,如 7d,将来可能会进一步开发为有效的、选择性的抗肿瘤药物,以潜在地规避多药耐药(MDR)。