Skip to main content
. 2017 Nov 9;8(63):107134–107148. doi: 10.18632/oncotarget.22359

Figure 5. Transcriptional repression of ESR1 by DDIT3.

Figure 5

Immunoblotting (A) and RT-qPCR (B) analyses of DDIT3 and ERα levels in BCa cells treated with DDIT3 shRNA or negative control. (C) Effect of combined treatment with DDIT3 shRNA and PD98059 on ERα levels in MCF7/LR cells. 48 h after transfection with pLenti-DDIT3 or empty vector, MCF7 cells were subjected to immunoblotting (D) or RT-qPCR (E) analyses of DDIT3 and ERα expression. (F) DDIT3 directly targets the ESR1 promoter in a luciferase reporter assay. (G) Simplified structure of the potential binding site of DDIT3 onto ESR1 promoter. (H) ChIP analysis showing recruitment of DDIT3 onto a specific region of the ESR1 promoter in MCF7 cells. (I) ChIP analysis showing that letrozole treatment could enhance the recruitment of DDIT3 onto ESR1 promoter and mutation of DDIT3 binding sites in the ESR1 promoter region substantially abolished the recruitment.