Mitochondrial depolarization and apoptosis associated with sustained activation of c-jun-N-terminal kinasein the human multiple myeloma cell line U266 induced by 2-aminophenoxazine-3-one
- Authors:
- Published online on: March 1, 2009 https://doi.org/10.3892/mmr_00000084
- Pages: 199-203
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
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.
