Figure 3
CFZ blocks HDACI-mediated NF-κB activation in both SUDHL4 and OCI-LY10 DLBCL cells. (A) SUDHL4 DLBCL cells were treated with CFZ (4.0nM) with or without vorinostat (1.5μM), and (B) OCI-LY10 DLBCL cells were treated with CFZ (7.0nM) with or without vorinostat (1.5μM) for 18 hours. Nuclear protein was extracted using Nuclear Extract Kit (Active Motif), and NF-κB activity was determined using an ELISA TransAM NF-κB p65 Transcription Factor Assay Kit (Active Motif), as described in “NF-κB activity.” Inset: After identical treatment, the same nuclear proteins were subjected to EMSA gel shift assays to assess NF-κB DNA binding as described in “NF-κB activity.” Values represent the means for triplicate determinations for 3 separate experiments. *Significantly less than values for vorinostat alone (P < .002).

CFZ blocks HDACI-mediated NF-κB activation in both SUDHL4 and OCI-LY10 DLBCL cells. (A) SUDHL4 DLBCL cells were treated with CFZ (4.0nM) with or without vorinostat (1.5μM), and (B) OCI-LY10 DLBCL cells were treated with CFZ (7.0nM) with or without vorinostat (1.5μM) for 18 hours. Nuclear protein was extracted using Nuclear Extract Kit (Active Motif), and NF-κB activity was determined using an ELISA TransAM NF-κB p65 Transcription Factor Assay Kit (Active Motif), as described in “NF-κB activity.” Inset: After identical treatment, the same nuclear proteins were subjected to EMSA gel shift assays to assess NF-κB DNA binding as described in “NF-κB activity.” Values represent the means for triplicate determinations for 3 separate experiments. *Significantly less than values for vorinostat alone (P < .002).

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