Abstract
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.
| Original language | English |
|---|---|
| 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 |
ASJC Scopus Subject Areas
- Hematology
- Oncology
- Cancer Research
Keywords
- Apoptosis
- Bax
- Etoposide
- Lipopolysaccharide
- NF-κB
- THP-1 cells
- XIAP
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