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.
- Hodgkin's lymphoma
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