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核因子-κB（NF-κB）与p38丝裂原活化蛋白激酶（p38 MAPK）的平衡是AML-2及其阿霉素耐药细胞系放射敏感性的决定因素。

Balance of NF-kappaB and p38 MAPK is a determinant of radiosensitivity of the AML-2 and its doxorubicin-resistant cell lines.

作者信息

Choi Cheol-Hee, Xu Haidong, Bark Hyun, Lee Tae-Bum, Yun Jisoo, Kang Sung-In, Oh Yoon-Kyeong

机构信息

Research Center for Resistant Cells, Chosun University, Gwangju 501-759, Republic of Korea.

出版信息

Leuk Res. 2007 Sep;31(9):1267-76. doi: 10.1016/j.leukres.2006.11.006. Epub 2007 Jan 10.

DOI:10.1016/j.leukres.2006.11.006
PMID:17218010
Abstract

This study investigated radioresistance mechanisms in the doxorubicin-resistant acute myelogenous leukemia (AML)-2/DX100. AML-2/DX100 also showed resistance to radiation. AML-2/DX100 characterized by down-regulated catalase expression was supersensitive to exogenous hydrogen peroxide whereas they increased defense mechanisms against endogenous reactive oxygen species (ROS) as compared with AML-2/WT. In AML-2/WT, radiation increased Bax expression and its translocation to mitochondria but had little effect on translocation of Bcl-2 and consequently induced the release of cytochrome c from the mitochondria with the subsequent caspase-3 activation. On the contrary, in AML-2/DX100, radiation neither increased Bax expression nor its translocation to mitochondria while it increased Bcl-2 translocation to mitochondria. A specific p38 MAPK inhibitor SB203580 increased radioresistance in AML-2/WT but little in AML-2/DX100. It inhibited radiation-induced Bax translocation in AML-2/WT but not in AML-2/DX100, indicating that p38 MAPK is working after irradiation in AML-2/WT but not in AML-2/DX100. Electrophoretic mobility shift assay and Western blot analysis revealed that NF-kappaB in AML-2/DX100 was more activated with degradation of cytosolic IkappaBalpha than was that of AML-2/WT. cDNA microarray showed that Bfl-1/A1 and granzyme H in AML-2/DX100 were highly up-regulated (6.21-fold) and down-regulated (6.49-fold), respectively, as compared with each of AML-2/WT, which were confirmed by RT-PCR assay. Taken together, these results indicate that radioresistance mechanisms of AML-2/DX100 could be related to alterations in ROS-scavenging activity, in mitochondrial translocation of Bax and Bcl-2, and in expression of pro-apoptotic (granzyme H) and anti-apoptotic (Bfl-1/A1) genes. It has been shown that balance of p38 MAPK and NF-kappaB signals is a determinant in radiosensitivity of AML-2/WT and AML-2/DX100.

摘要

本研究调查了多柔比星耐药急性髓性白血病（AML）-2/DX100中的辐射抗性机制。AML-2/DX100也表现出对辐射的抗性。AML-2/DX100以过氧化氢酶表达下调为特征，对外源性过氧化氢超敏感，而与AML-2/WT相比，它们增强了对内源性活性氧（ROS）的防御机制。在AML-2/WT中，辐射增加了Bax的表达及其向线粒体的转位，但对Bcl-2的转位影响很小，因此诱导了细胞色素c从线粒体的释放，随后激活了caspase-3。相反，在AML-2/DX100中，辐射既没有增加Bax的表达也没有增加其向线粒体的转位，而增加了Bcl-2向线粒体的转位。一种特异性p38丝裂原活化蛋白激酶（MAPK）抑制剂SB203580增加了AML-2/WT中的辐射抗性，但对AML-2/DX100的作用很小。它抑制了AML-2/WT中辐射诱导的Bax转位，但对AML-2/DX100没有作用，表明p38 MAPK在AML-2/WT照射后起作用，而在AML-2/DX100中不起作用。电泳迁移率变动分析和蛋白质免疫印迹分析显示，与AML-2/WT相比，AML-2/DX100中的核因子κB（NF-κB）因胞质IκBα降解而更易被激活。基因芯片显示与AML-2/WT相比，AML-2/DX100中的Bfl-1/A1和颗粒酶H分别高度上调（6.21倍）和下调（6.49倍），这通过逆转录聚合酶链反应（RT-PCR）分析得到证实。综上所述，这些结果表明AML-2/DX100的辐射抗性机制可能与ROS清除活性、Bax和Bcl-2的线粒体转位以及促凋亡基因（颗粒酶H）和抗凋亡基因（Bfl-1/A1）的表达改变有关。已表明p38 MAPK和NF-κB信号的平衡是AML-2/WT和AML-2/DX100放射敏感性的决定因素。

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