Dual role of NF-κB in apoptosis of THP-1 cells during treatment with etoposide and lipopolysaccharide

Keiko Sato, Takahiro Taniguchi, Maiko Suzuki, Fumiaki Shinohara, Haruhiko Takada, Hidemi Rikiishi

Research output: Contribution to journalArticle

8 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)63-69
Number of pages7
JournalLeukemia Research
Volume28
Issue number1
DOIs
StatePublished - Jan 1 2004
Externally publishedYes

Fingerprint

Etoposide
Lipopolysaccharides
Apoptosis
X Chromosome
Dactinomycin
Cycloheximide
Ketones
Cell Survival
Genes
Neoplasms

Keywords

  • Apoptosis
  • Bax
  • Etoposide
  • Lipopolysaccharide
  • NF-κB
  • THP-1 cells
  • XIAP

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Cite this

Dual role of NF-κB in apoptosis of THP-1 cells during treatment with etoposide and lipopolysaccharide. / Sato, Keiko; Taniguchi, Takahiro; Suzuki, Maiko; Shinohara, Fumiaki; Takada, Haruhiko; Rikiishi, Hidemi.

In: Leukemia Research, Vol. 28, No. 1, 01.01.2004, p. 63-69.

Research output: Contribution to journalArticle

Sato, Keiko ; Taniguchi, Takahiro ; Suzuki, Maiko ; Shinohara, Fumiaki ; Takada, Haruhiko ; Rikiishi, Hidemi. / Dual role of NF-κB in apoptosis of THP-1 cells during treatment with etoposide and lipopolysaccharide. In: Leukemia Research. 2004 ; Vol. 28, No. 1. pp. 63-69.
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