Modulation of transcription factor NF-kappaB in Hodgkin's lymphoma cell lines: effect of (-)-epicatechin.
Transcription factor NF-kappaB 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-kappaB activation in Jurkat T cells. Therefore, we investigated the capacity of EC to inhibit NF-kappaB activation, the underlying mechanisms and the effects of EC on cell viability in Hodgkin's lymphoma cells. EC inhibited NF-kappaB-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-kappaB nuclear translocation. Results suggest that EC acted inhibiting the binding of NF-kappaB to DNA. The combined treatment with EC and an inhibitor of NF-kappaB nuclear translocation (SN-50) caused an additive inhibitory effect on NF-kappaB activation. The partial cell viability decrease, under conditions that EC and SN-50 completely prevented NF-kappaB-DNA binding, indicates that the inhibition of other signaling pathways should be also targeted in the treatment of Hodgkin's lymphoma.
Mackenzie
Gerardo G
GG
Department of Nutrition, University of California Davis, Davis, CA 95616, USA.
Oteiza
Patricia I
PI
D002392:Catechin / Q000494:pharmacology*; D045744:Cell Line, Tumor; D004247:DNA / Q000378:metabolism; D006689:Hodgkin Disease / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D016328:NF-kappa B / Q000819:agonists / Q000037:antagonists & inhibitors* / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D021381:Protein Transport / Q000187:drug effects; D008063:Thioctic Acid / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects
D016328:NF-kappa B; D016877:Oxidants; D010455:Peptides; C118258:SN50 peptide; D008063:Thioctic Acid; D002392:Catechin; D004247:DNA