Figure 2.
Figure 2. Multiple myeloma cell lines respond differently to direct inhibition of NF-κB than they do to direct inhibition of the 26S proteasome. (A) Whole-cell lysates were prepared from untreated multiple myeloma cell lines, cells treated with 5 μM BAY 11-7082 or cells treated with 100 nM (8226/S and U266 cells), 25 nM (KMS-11, KMS-18), or 5 nM (MM.1S) bortezomib and incubated with a double-stranded NF-κB oligonucleotide probe. Samples were run on a native polyacrylamide gel, and NF-κB binding was visualized by autoradiography. (B) Five different human multiple myeloma cell lines were cultured for 24 hours in increasing concentrations of the NF-κB inhibitor BAY 11-7082. Cell viability, as assessed by Annexin V–FITC and propidium iodide staining, is presented as the mean ± SD from at least 3 independent experiments.

Multiple myeloma cell lines respond differently to direct inhibition of NF-κB than they do to direct inhibition of the 26S proteasome. (A) Whole-cell lysates were prepared from untreated multiple myeloma cell lines, cells treated with 5 μM BAY 11-7082 or cells treated with 100 nM (8226/S and U266 cells), 25 nM (KMS-11, KMS-18), or 5 nM (MM.1S) bortezomib and incubated with a double-stranded NF-κB oligonucleotide probe. Samples were run on a native polyacrylamide gel, and NF-κB binding was visualized by autoradiography. (B) Five different human multiple myeloma cell lines were cultured for 24 hours in increasing concentrations of the NF-κB inhibitor BAY 11-7082. Cell viability, as assessed by Annexin V–FITC and propidium iodide staining, is presented as the mean ± SD from at least 3 independent experiments.

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