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Fig. 3 | Molecular Cancer

Fig. 3

From: RIPK3 activation induces TRIM28 derepression in cancer cells and enhances the anti-tumor microenvironment

Fig. 3

TRIM28 antagonizes NF-κB transactivation independent of p65 chromatin occupancy. (A) HA-p65 vector was transiently co-transfected with various doses of Flag-TRIM28 in 293 T cells. After 24 h, luciferase assays were performed, and the activity of each sample was normalized to Renilla activity. (B) 293A and HT-29 cells were transiently transfected with Myc-TRIM28 or HA-TRIM28 for 24 h. Cell lysates were subjected to western blotting. (C and D) 293A or HT-29 cells were transiently transfected with the TRIM28 vector. After 24 h, IL-8, CXCL1 and TNF-α mRNA levels were measured by qPCR. (E and F) HT-29 or HeLa (RIPK3) cells were transiently transfected with the TRIM28 vector. After 24 h, cells were treated with TSZ for the indicated times. Cell lysates were subjected to western blotting (right), and mRNA levels were determined by qPCR (left). (G) Metagene representation of the ChIP-seq signal for TRIM28 across 9412 TRIM28-occupied regions in HT-29 cells treated with TNF-α or TSZ for 4 h. Metagenes centered on the middle of the 9412 regions and 10 Kb around the center of the regions are displayed. (H) Metagene representation of the ChIP-seq signal for TRIM28 across 497 regions and 163 genes-associated peaks in HT-29 cells treated with TNF-α or TSZ for 4 h. Metagenes centered on the middle of 497 regions and 10 Kb around the center of 497 regions are displayed. (I) ChIP-seq profiles of p65 and TRIM28 in HT-29 cells treated with TNF-α or TSZ for 4 h at the CSF1 and IL32 loci

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