Dexamethasone decreases expression of c-maf and its target genes in multiple myeloma cell lines. LP-1 myeloma cells that overexpress c-maf but lack the t(14;16) translocation (A) and RPMI 8226 myeloma cells that have the t(14;16) translocation (B) were treated with increasing concentrations of dexamethasone. After treatment, cell lysates were immunoblotted using antibodies specific for c-maf, cyclin D2, XIAP, Bcl-2, and β-actin. (C) Myeloma cell lines were treated with dexamethasone (5 μmol/L) or buffer control for 24 hours. Total cell lysates were immunoblotted using antibodies specific for c-maf, cyclin D2, and β-actin. (D) MM1.S and the paired cell line MM1.R that lacks the glucocorticoid receptor were treated with dexamethasone (5 μmol/L). At increasing times after treatment, cell lysates were immunoblotted using antibodies specific for c-maf, cyclin D2, and β-actin. (E) MM1.S (glucocorticoid sensitive) and the paired cell line glucocorticoid-resistant MM1.R were treated with dexamethasone (DEX; 5 μmol/L) for 48 hours. After incubation, β-integrin-7 surface expression was measured by staining cells with anti-β–integrin-7-FITC, and flow cytometric analysis was performed. (F) Myeloma cell lines were treated with increasing concentrations of dexamethasone. Cell viability was measured 48 hours later by MTS assay. Cell viability is expressed as a mean percentage (± SD; n = 3) relative to untreated cells. (G) MM1.S cells were transfected with cDNA corresponding to cyclin D2 or empty vector. Twenty-four hours after transfection, cells were treated with increasing concentrations of dexamethasone for 24 hours. Cell viability was measured by MTS assay and expressed as a mean percentage (± SD; n = 3) relative to control cells. Inset: expression of cyclin D2 and β-actin by immunoblotting cell lysates from MM1.S cells transfected with cyclin D2 or empty vector.