Takasaki Akira, Hanyu Haruo, Iwamoto Toshihiko, Shirato Ken, Izumi Ryutaro, Toyota Hiroko, Mizuguchi Junichiro, Miyazawa Keisuke, Tomoda Akio
Department of Geriatric Medicine, Tokyo Medical University, Tokyo 160-0023, Japan.
Mol Med Rep. 2009 Mar-Apr;2(2):199-203. doi: 10.3892/mmr_00000084.
We investigated the involvement of c-jun-N-terminal kinase (JNK) in mitochondrial depolarization and apoptosis in a human multiple myeloma cell line, U266, treated with 2-aminophenoxazine (Phx-3). It was found that, with Phx-3 administration to U266 cells, JNK was phosphorylated 2 and 7.5-fold at 6 and 24 h, respectively, compared to the Phx-3-free control. This increasing activation of JNK in U266 cells with Phx-3 correlated with cellular disorders, such as mitochondrial depolarization and cellular apoptosis. When the JNK-specific inhibitor SP6000125 was administered to the U266 cells together with Phx-3, the number of cells exhibiting mitochondrial depolarization and cellular apoptosis was significantly reduced. These results suggest that JNK activation in human multiple myeloma U266 cells may be closely associated with mitochondrial depolarization and apoptosis.
我们研究了c-jun氨基末端激酶（JNK）在2-氨基吩恶嗪（Phx-3）处理的人多发性骨髓瘤细胞系U266的线粒体去极化和凋亡过程中的作用。结果发现，在U266细胞中给予Phx-3后，与未给予Phx-3的对照组相比，JNK在6小时和24小时时分别被磷酸化2倍和7.5倍。随着Phx-3处理，U266细胞中JNK的这种激活增加与细胞紊乱相关，如线粒体去极化和细胞凋亡。当JNK特异性抑制剂SP6000125与Phx-3一起给予U266细胞时，表现出线粒体去极化和细胞凋亡的细胞数量显著减少。这些结果表明，人多发性骨髓瘤U266细胞中的JNK激活可能与线粒体去极化和凋亡密切相关。
