作者: Feng-hao Xu , Sanjesh Sharma , Agnes Gardner , Yiping Tu , Arthur Raitano
DOI: 10.1182/BLOOD.V92.1.241.413K28_241_251
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摘要: The mechanism by which interleukin-6 (IL-6) protects multiple myeloma (MM) plasma cells from apoptosis induced anti-fas antibodies and dexamethasone was studied. Anti-apoptotic concentrations of IL-6 had no effect on cell-cycle distribution or activation RAF-1 ERK in dexamethasone- anti-fas-treated 8226 UCLA #1 MM cell lines. However, IL-6-dependent protection viability correlated with an inhibition anti-fas-induced jun kinase (JNK) AP-1 transactivation. To test the hypothesis that cytokine-induced mediated through JNK/c-jun, we also inhibited c-jun function via introduction a mutant dominant negative construct. Mutant c-jun-containing were resistant to but significantly more sensitive dexamethasone-induced apoptosis. These results support notion against its inhibitory effects JNK/c-jun indicate occurs separate, yet unknown pathways.