Fig. 5
A A predictive interactome map of ITGB7 was constructed with STRING protein network analysis (confidence ≥ 9.0), which showed strong involvement (FDR < 0.001) of the protein in functions such as cell matrix adhesion and migration, extracellular matrix interactions, cell–cell interactions, and focal adhesion. B MM.1S cells were treated with a bromodomain-4 (BRD4) inhibitory drug, JQ1, at concentrations ranging from 25 nM to 2 µM; half-life of inhibitory concentration (IC50) was recorded after 24 h, 48 h, and 72 h of incubation. C JQ1 treatment at 0.1 µM (IC50 at 24 h) and 0.2 µM (onefold higher than IC50 at 24 h) effectively reduced expression of super-enhancer–bound epigenetic marks, such as BRD4, MED1, or H3K27ac, with simultaneous reduction in expression of underlying genes, as exemplified with ITGB7. In contrast, expression of cMAF or endogenous controls (β-actin, H3) remained unaltered