期刊论文详细信息
Journal of Enzyme Inhibition and Medicinal Chemistry | |
Antiproliferative chromone derivatives induce K562 cell death through endogenous and exogenous pathways | |
Runwei Jiao1  Dahong Li1  Haonan Li1  Zhanlin Li1  Huiming Hua1  Xiaofang Huang1  Hao Cao2  Linghe Zang2  Weiwei Liu3  Fanxing Xu3  | |
[1]Key Laboratory of Structure-Based Drug Design and Discovery, Ministry of Education, School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University | |
[2]School of Life Science and Biopharmaceutics, Shenyang Pharmaceutical University | |
[3]Wuya College of Innovation, Shenyang Pharmaceutical University | |
关键词: chromone; nitric oxide; antiproliferative; selectivity; apoptosis; | |
DOI : 10.1080/14756366.2020.1740696 | |
来源: DOAJ |
【 摘 要 】
A series of furoxan derivatives of chromone were prepared. The antiproliferative activities were tested against five cancer cell lines HepG2, MCF-7, HCT-116, B16, and K562, and two normal human cell lines L-02 and PBMCs. Among them, compound 15a exhibited the most potent antiproliferative activity. It was also found 15a produced more than 8 µM of NO at the peak time of 45 min by Griess assay. Generally, antiproliferative activity is positively related to NO release to some extent. Further in-depth studies on apoptosis-related mechanisms showed that 15a caused S-phase cell cycle arrest in a concentration-dependent manner and induced apoptosis significantly through mitochondria-related pathways. Human apoptosis protein array assay also demonstrated 15a increased the expression levels of pro-apoptotic Bax, Bad, HtrA2 and Trail R2/DR5. The expression of catalase and cell cycle blocker claspin were similarly up-regulated. In balance, 15a induced K562 cells death through both endogenous and exogenous pathways.【 授权许可】
Unknown