Specific killing of CCR9 high-expressing acute T lymphocytic leukemia cells by CCL25 fused with PE38 toxin
Specific killing of CCR9 high-expressing acute T lymphocytic leukemia cells by CCL25 fused with PE38 toxin
复制标题
CCL25与PE38毒素融合对CCR9高表达急性T淋巴细胞白血病细胞的特异性杀伤作用。
DOI：
10.1016/j.leukres.2011.01.015
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发表时间：
2011-09-01
影响因子：
2.7
通讯作者：
Zhang, Qiuping
中科院分区：
文献类型：
--
作者：
Hu, Yi;Zhang, Li;Zhang, Qiuping
我们以前已经证明，CCR 9在人类急性T淋巴细胞白血病（T-ALL）的耐药性和侵袭中起着关键作用。在这项研究中，我们研究了MOLT 4细胞，自然表达CCR 9在高水平，是否可以成功地杀死特定的配体，CCL 25融合到假单胞菌外毒素38（PE 38）毒素。我们的研究结果表明，CCL 25-PE 38能够通过诱导凋亡特异性地杀死MOLT 4细胞，并抑制CCR 9（+）肿瘤的生长。这项工作表明，CCR 9高表达的人T-ALL细胞可以通过递送与配体CCL 25融合的PE 38毒素成功杀死。(C)2011爱思唯尔有限公司版权所有。
We have previously demonstrated that CCR9 plays a pivotal role in drug resistance and invasion in human acute T-lymphocytic leukemia (T-ALL). In this study, we investigated whether the MOLT4 cells, which naturally express CCR9 at high levels, can be successfully killed by the specific ligand, CCL25 fused to Pseudomonas exotoxin 38 (PE38) toxin. Our results demonstrated that CCL25-PE38 was able to specifically kill MOLT4 cells via apoptosis induction, and suppress the growth of CCR9(+) tumors. This work shows that CCR9 high-expressing human T-ALL cells can be successfully killed by delivering PE38 toxin fused to the ligand CCL25. (C) 2011 Elsevier Ltd. All rights reserved.