c-Jun氨基末端激酶2（JNK2）在对维生素D耐药的人髓系白血病细胞中拮抗JNK1的分化信号。
c-Jun N-terminal kinase 2 (JNK2) antagonizes the signaling of differentiation by JNK1 in human myeloid leukemia cells resistant to vitamin D.
作者信息
Chen-Deutsch Xiangwen, Garay Edward, Zhang Jing, Harrison Jonathan S, Studzinski George P
机构信息
Department of Pathology and Laboratory Medicine, UMDNJ-New Jersey Medical School, 185 So. Orange Avenue, Newark, NJ 07103, USA.
出版信息
Leuk Res. 2009 Oct;33(10):1372-8. doi: 10.1016/j.leukres.2009.03.003. Epub 2009 Mar 31.
Abstract
1,25-Dihydroxyvitamin D3 (1,25D) induces differentiation of myeloid leukemia cells, but resistant cells are also encountered. We studied the mechanistic basis for the resistance in a model system using enhancers of 1,25D, the antioxidant carnosic acid and a kinase inhibitor SB202190. Knock-down (KD) of JNK2p54 unexpectedly increased the intensity of differentiation induced by the 1,25D, carnosic acid and SB202190 (DCS) combination. This was associated with upregulation of activated JNK1p46, and the transcription factors regulated by the JNK pathway, c-Jun, ATF2 and JunB, as well as C/EBP beta. In contrast, KD of JNK1p46 reduced the intensity of DCS-induced differentiation, and partially abrogated activation of c-Jun/AP-1 transcription factors.
摘要
1,25-二羟基维生素D3（1,25D）可诱导髓系白血病细胞分化，但也会出现耐药细胞。我们在一个模型系统中研究了耐药的机制基础，该模型使用了1,25D的增强剂、抗氧化剂肌醇六磷酸和激酶抑制剂SB202190。意外的是，JNK2p54的敲低（KD）增加了1,25D、肌醇六磷酸和SB202190（DCS）组合诱导的分化强度。这与活化的JNK1p46以及由JNK途径调节的转录因子c-Jun、ATF2和JunB以及C/EBPβ的上调有关。相反，JNK1p46的KD降低了DCS诱导的分化强度，并部分消除了c-Jun/AP-1转录因子的活化。
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