Fig. 6

The clinical significance of c-Myc and the mechanism of BRD7 and c-Myc in NPC progression. a The expression of c-Myc, BRD7 and miR-141 was analyzed by IHC or ISH in NPC (Tumor, N = 41) and non-cancerous nasopharyngeal controls (non-Tumor, N = 27), respectively. Original magnification, 200×; the scale bars represent 50 μm. b Box diagram of c-Myc, BRD7 and miR-141 expression in NPC and non-cancerous nasopharyngeal control tissues. The whiskers represent the minimum and maximum values for each group. **P < 0.01, ***P < 0.001. c A schematic map showing the mechanism of the negative feedback loop between BRD7 and c-Myc in miR-141 transcription that contributes to NPC cell proliferation and survival. In this model, c-Myc binds directly to the BRD7 promoter and represses its transcription; meanwhile, BRD7 interacts with c-Myc and functions as a cofactor of c-Myc in the transcription of miR-141, which induces the inhibition of miR-141 transcription; miR-141 activates the AKT pathway through directly targeting PTEN and then promotes the cell proliferation and survival of NPC