BRD4 interacts with PML/RARα in acute promyelocytic leukemia

bromodomain-containing 4 (brd4) has been considered as an important requirement for disease maintenance and an attractive therapeutic target for cancer therapy. this protein can be targeted by jq1, a selective small-molecule inhibitor. however, few studies have investigated whether brd4 influenced acute promyelocytic leukemia (apl), and whether brd4 had interaction with promyelocytic leukemia-retinoic acid receptor α (pml/rarα) fusion protein to some extent. results from cell viability assay, cell cycle analysis, and annexin-v/pi analysis indicated that jq1 inhibited the growth of nb4 cells, an apl-derived cell line, and induced nb4 cell cycle arrest at g1 and apoptosis. then, we used co-immunoprecipitation (co-ip) assay and immunoblot to demonstrate the endogenous interaction of brd4 and pml/rarα in nb4 cells. moreover, downregulation of pml/rarα at the mrna and protein levels was observed upon jq1 treatment. furthermore, results from the rt-qpcr, chip-qpcr, and re-chip-qpcr assays showed that brd4 and pml/rarα co-existed on the same regulatory regions of their target genes. hence, we showed a new discovery of the interaction of brd4 and pml/rarα, as well as the decline of pml/rarα expression, under jq1 treatment.