Methylation of the DPH1 promoter causes immunotoxin resistance in acute lymphoblastic leukemia cell line KOPN-8

被引：18
作者：
Hu, Xiaobo [1 ]
Wei, Hui [1 ]
Xiang, Laiman [1 ]
Chertov, Oleg [2 ]
Wayne, Alan S. [1 ,3 ]
Bera, Tapan K. [1 ]
Pastan, Ira [1 ]
机构：
[1] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA
[2] NCI, Prot Chem Lab, Adv Technol Program, SAIC Frederick,Frederick Natl Lab Canc Res, Frederick, MD 21701 USA
[3] NCI, Pediat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA
来源：
LEUKEMIA RESEARCH | 2013年 / 37卷 / 11期
关键词：
DNA methylation; Drug resistance; ADP-ribosylation; Diphthamide synthesis; Epigenetic regulation; PSEUDOMONAS-EXOTOXIN; DIPHTHAMIDE BIOSYNTHESIS; DIPHTHERIA-TOXIN; GENE; 5-AZA-2'-DEOXYCYTIDINE; EXPRESSION; APOPTOSIS; THERAPY;
D O I：
10.1016/j.leukres.2013.08.005
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Moxetumomab pasudotox (HA22) is an immunotoxin with an anti-CD22 Fv fused to a portion of Pseudomonas exotoxin A that kills CD22 expressing ALL cells. HA22 produced significant responses in some cases of ALL. To understand how to increase response rate, we isolated HA22-resistant KOPN-8 cells and found that HA22 cannot inactivate elongation factor-2 (EF2) due to low levels of DPH1 RNA and protein. Resistance was associated with methylation of the CpG island in the DPH1 promoter. 5-Azacytidine prevented resistance and methylation of the CpG residues and merits evaluation to determine if it can increase the efficacy of HA22 in ALL. Published by Elsevier Ltd.
引用
收藏
页码：1551 / 1556
页数：6
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