Modulation of transcription factor NF-κB in Hodgkin's lymphoma cell lines: Effect of (-)-epicatechin

Gerardo Mackenzie, Patricia I. Oteiza

Research output: Contribution to journalArticle

42 Scopus citations

Abstract

Transcription factor NF-κB plays a central role in tumorogenesis and in different types of cancer, including Hodgkin's lymphoma. Previously, we described that (-)-epicatechin (EC) inhibits PMA-induced NF-κB activation in Jurkat T cells. Therefore, we investigated the capacity of EC to inhibit NF-κB activation, the underlying mechanisms and the effects of EC on cell viability in Hodgkin's lymphoma cells. EC inhibited NF-κB-DNA binding activity in L-428 and KM-H2 cells. This inhibition was not associated with EC antioxidant activity, with changes in p65 phosphorylation or NF-κB nuclear translocation. Results suggest that EC acted inhibiting the binding of NF-κB to DNA. The combined treatment with EC and an inhibitor of NF-κB nuclear translocation (SN-50) caused an additive inhibitory effect on NF-κB activation. The partial cell viability decrease, under conditions that EC and SN-50 completely prevented NF-κB-DNA binding, indicates that the inhibition of other signaling pathways should be also targeted in the treatment of Hodgkin's lymphoma.

Original languageEnglish (US)
Pages (from-to)1086-1094
Number of pages9
JournalFree Radical Research
Volume40
Issue number10
DOIs
StatePublished - Oct 2006

Keywords

  • (-)-epicatechin
  • Flavonoids
  • Hodgkin's lymphoma
  • NF-κB
  • SN-50

ASJC Scopus subject areas

  • Biochemistry

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