Ceap/BLOS2 interacts with BRD7 and selectively inhibits its transcription-suppressing effect on cellular proliferation-associated genes.

The centrosome associated protein Ceap-16 (also termed BLOS2) can accelerate the proliferation of mouse fibroblast NIH3T3 cells, which mechanism remains unclear. Here we identified tumor suppressor candidate BRD7 (bromodomain containing protein 7), which could negatively regulate cell proliferation and growth, as a novel Ceap-16-interacting protein. Ceap-16 and BRD7 interacted with each other both in vitro and in vivo. The C-terminus of BRD7 and the central region of Ceap-16 mediated the interaction. Through this binding, Ceap-16 could translocate from cytoplasm to the nucleus where it selectively inhibited the transcriptional suppression activity of BRD7 towards certain target genes including E2F3 and cyclin A. Moreover, Ceap-16, BRD7 and histone H3/H4 could form a complex and Ceap-16 did not compete with BRD7 binding to histones. These findings suggest a novel function for Ceap-16 in the transcriptional regulation through associating with BRD7.