One of the mechanisms repressing apoptosis in tumor cells can involve the expression of anti-apoptotic NF-κB target genes. In this study, we demonstrated that a potent NF-κB inhibitor, Nα-tosyl-L-lysinyl chloromethyl ketone (TLCK), inhibits apoptosis of THP-1 cells triggered by etoposide (VP16), and actinomycin D (ACT D) or cycloheximide inhibits apoptosis. However, persistent activation of NF-κB by lipopolysaccharide (LPS) led to the survival of leukemic cells against VP16-induced apoptosis. Thus, the molecular events (Bax/X-chromosome-linked IAP (XIAP)) occurring downstream of NF-κB activation during VP16 and/or LPS stimulation may become important to understand the multiple effects of NF-κB.
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