Abstract
One of the mechanisms repressing apoptosis in tumor cells can involve the expression of anti-apoptotic NF-kappaB target genes. In this study, we demonstrated that a potent NF-kappaB inhibitor, Nalpha-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-kappaB 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-kappaB activation during VP16 and/or LPS stimulation may become important to understand the multiple effects of NF-kappaB.
Original language | English (US) |
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Pages (from-to) | 63-69 |
Number of pages | 7 |
Journal | Leukemia Research |
Volume | 28 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2004 |
Externally published | Yes |
Keywords
- Apoptosis
- Bax
- Etoposide
- Lipopolysaccharide
- NF-κB
- THP-1 cells
- XIAP
ASJC Scopus subject areas
- Hematology
- Oncology
- Cancer Research