文献类型：期刊文献

英文题名：7-b, a novel amonafide analogue, cause growth inhibition and apoptosis in Raji cells via a ROS-mediated mitochondrial pathway

作者：Lin, Bing[1,2];Chen, Zhuo[1,2];Xu, Yufang[1,2];Zhang, Huanying[1,2];Liu, Jianwen[1,2];Qian, Xuhong[1,2]

机构：[1]E China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, 268,130 Meilong Rd, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab Chem Biol, Shanghai 200237, Peoples R China

年份：2011

卷号：35

期号：5

起止页码：646

外文期刊名：LEUKEMIA RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000289549500030)】；

基金：This work was supported by Shanghai Leading Academic Discipline Project, Project No. B507, the National Special Fund for State Key Laboratory of Bioreactor Engineering, Grant No. 2060204 and the 111 Project, Grant No. B07023.

语种：英文

外文关键词：7-b; Cell cycle; Apoptosis; Reactive oxygen species; Mitochondrial membrane potential; p21

摘要：Previous studies have shown that 7-b (6-(dodecylamino)-2-(3-(4-methylpiperazin-1-yl)propyl)-1H-benzo-[de]isoquinoline-1,3(2H)-dione), a novel amonafide-based DNA intercalator, was generated as a new anticancer candidate. However, the effects induced by 7-b and the molecular mechanisms involved remain poorly understood in Burkitt's lymphoma. To shed light on these issues, we have investigated the effects of 7-b on proliferation, cell cycle progression, apoptosis activity and oxidative stress levels of lymphoma Raji cells in vitro. Our results showed that 7-b inhibited the proliferation of Raji cells and induced G1 cell cycle arrest in a dose-dependent manner. Moreover, 7-b treatment triggered programmed cell death, production of reactive oxygen species (ROS) and alteration of the mitochondrial membrane potential (Delta psi m). Altogether our results showed that 7-b mediated its growth inhibitory effects on Raji cells via the activation of a ROS-mediated mitochondrial pathway and cell cycle checkpoint signaling pathway which subsequently targeted p21. (C) 2011 Elsevier Ltd. All rights reserved.