TNF increases camptothecin-induced apoptosis by inhibition of NF-κB

P. Valente, D. Arzani, A. Cesario, S. Margaritora, E. Carbone, P. Russo

Research output: Contribution to journalArticlepeer-review


rHuTNF potentiates CPT-cytotoxicity in human ovarian A2780 cells. In this study, we examined the role of NF-κB in this potentiation. A pulse-labelled DNA study indicated that the combination CPT+TNF had little effect on the rate of DNA elongation at 6 h after drug removal, whereas CPT alone produced a complete inhibition for at least 6 h after drug removal. Flow cytometry analyses showed that CPT+TNF arrested cells in the G 2-M phase, whereas CPT blocked cells in S phase. Looking at the persistence of the NF-κB complexes in cells, it appeared that they were still present at 24 h in TNF-treated cells. In contrast, in CPT-treated cells they persisted for 6 h. In CPT+TNF-treated cells, the NF-κB complexes disappeared quickly and became undetectable at 6 h. The induction of apoptosis was detected only in the CPT+TNF treated cells (using flow cytometry, a filter binding assay and ApopTag staining). These findings show that TNF, in combination with CPT, reduces the time that NF-κB complexes persist in cells likely resulting in the induction of apoptosis.

Original languageEnglish
Pages (from-to)1468-1477
Number of pages10
JournalEuropean Journal of Cancer
Issue number10
Publication statusPublished - Jul 2003


  • Apoptosis
  • Camptothecin
  • Cytotoxicity
  • DNA elongation
  • DNA synthesis cell cycle
  • NF-κB
  • Ovarian cancer cells
  • TNF

ASJC Scopus subject areas

  • Cancer Research
  • Hematology
  • Oncology


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