Studies showed that the bromodomain binds to acetyl-lysines on histone tails, 
which is involved in deciphering the histone codes. BRD7, a novel bromodomain 
gene, is the first described bromodomain gene involved in nasopharyngeal 
carcinoma (NPC). Previous studies showed that ectopic expression of BRD7 
inhibited cell growth and cell cycle progression from G1 to S phase in HNE1 
cells (a NPC cell line) by transcriptionally regulating some cell cycle related 
genes including E2F3 gene. In the present study, we revealed the co-localization 
between acetylated H3 and BRD7 and found that the bromodomain of BRD7 is 
required for this co-localization. More importantly, wild-type BRD7 interacted 
with H3 peptide acetylated at Lys14, while the bromodomain deleted mutant lost 
this ability. We also found that the mutant BRD7 failed to regulate E2F3 
promoter activity and inhibit cell cycle progression. These results indicated 
that the transcriptional regulation role of BRD7 was achieved by binding to 
acetylated histone H3 and that the bromodomain was essential for this role. In 
addition, no obvious changes were observed in the acetylated level of histone H3 
after transfection with BRD7, indicating that chromatin remodeling, not 
chromatin modification, is the major mechanism of BRD7 mediated gene 
transcription. Taken together, the present work shed light on the fact that a 
novel bromodomain gene, BRD7, is of importance in transcriptional regulation and 
cellular events including cell cycle.