RNA-seq of OPM2 multiple myeloma cells treated with HDAC inhibitors panobinostat, romidepsin, and ricolinostat.

Histone deacetylase (HDAC) inhibitors have been reported to exert synergistic antitumor effects with immunomodulatory drugs (IMiDs) in multiple myeloma, although the underlying molecular mechanisms are not fully elucidated. To delineate pathways potentially involved in this synergy, we profiled gene expression changes induced by HDAC inhibition in the OPM2 multiple myeloma cell line. Cells were treated with panobinostat (10 nM), romidepsin (10 nM), or ricolinostat (100 nM) for 2, 5, or 20 hours, followed by RNA-seq analysis. Two independent biological replicates were generated for each condition. These data provide a resource for identifying HDAC inhibitor–responsive genes and pathways that may contribute to the cooperative activity of HDAC inhibitors and IMiDs in multiple myeloma. Overall design: We analyzed the transcriptomes of OPM2 multiple myeloma cells treated with three histone deacetylase (HDAC) inhibitors: panobinostat (10 nM), romidepsin (10 nM), and ricolinostat (100 nM). Cells were harvested after 2, 5, and 20 hours of treatment. A vehicle control (DMSO) was included. For each condition, two independent biological replicates (n = 2) were generated.