Fig. 2

HDAC inhibitors enhance NKG2D ligand expression via a CRBN-independent pathway. a–c CRBN protein levels in RPMI8226, H929, and OPM-2 cells. The number below the band shows the density of CRBN normalized to that of actin. d–i MTT proliferation assay. Sensitivity of CRBN knockdown and CRBN-knockout MM cell lines to lenalidomide and pomalidomide. DMSO vehicle control and the corresponding values of MTT cell viability were designated as 100% (0 μM). To show whether inhibitors compromised cell proliferation of CRBN-knockdown cells, the ratio (%) of MTT cell viability for each concentration of lenalidomide or pomalidomide used, compared with DMSO vehicle control, is indicated. Each experiment was performed in quintuplicate (n = 5). Results are shown as the mean ± SD. (*p < 0.05, **p < 0.01, “ns” indicates no significant difference). j-m MICA and IKZF1 mRNA levels in CRBN-deficient RPMI8226 cells exposed to ACY-1215. Experiments were performed in triplicate (n = 3). (*p < 0.05, **p < 0.01, “ns” indicates no significant difference)