癸他滨
细胞凋亡
流式细胞术
淋巴母细胞
分子生物学
癌症研究
DNA损伤
白血病
生物
活力测定
化学
细胞培养
基因表达
DNA
基因
DNA甲基化
免疫学
生物化学
遗传学
作者
Pengcheng Shi,Leisi Zhang,Kai Chen,Zhiwu Jiang,Manman Deng,Jie Zha,Xutao Guo,Peng Li,Bing Xu
出处
期刊:Pharmacogenomics
[Future Medicine]
日期:2017-07-26
卷期号:18 (13): 1259-1270
被引量:18
标识
DOI:10.2217/pgs-2017-0061
摘要
To investigate the combined action of decitabine (DAC) with chidamide (CS055) on acute lymphoblastic leukemia (ALL) cells.ALL cell lines as well as primary cells from 17 ALL patients were subjected to different treatments and thereafter cell counting Kit-8 (CCK-8) assay, flow cytometry and western blot were employed to determine IC50, apoptosis and checkpoint kinase 1 and γH2A.X expression.Low-dose DAC combined with CS055 could effectively kill ALL cells by the reduction of cell viability and induction of apoptosis. This was also observed in primary cells from 17 ALL patients, especially for those with p16 gene deletion. Suppression of checkpoint kinase 1 phosphorylation and upregulation of γH2A.X expression was demonstrated to participate in DAC plus CS055-induced apoptosis.Low-dose DAC could enhance chidamide-induced apoptosis in adult ALL, especially for patients with p16 gene deletion through DNA damage.
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