Fig. 3: HSF1 chromatin occupancy and direct targets are reprogrammed in mCRPC cells.
From: HSF1–DBC1 axis drives prostate cancer progression by activating a metastatic transcriptional program

a ChIP-seq peak heights for each HSF1 binding site in 22RV1 under NHS and HS conditions and SM1 cells under NHS conditions. **P < 0.001. b, c Heat maps of HSF1 ChIP-seq signals in 22RV1 versus H1KO (b) under NHS and HS conditions and SM1 versus SM1-H1KO (c) under NHS conditions. The signals within 3 kb around the center of HSF1 ChIP-seq peaks are ordered by the decreasing ChIP-seq signal in SM1 cells. d Heat maps showing changes in ChIP-seq signals of HSF1 in 22RV1 versus SM1 cells. e A MEME-ChIP motif analysis reveals the top enriched motifs in HSF1 binding sites in SM cells. f The genomic distribution of HSF1 ChIP-seq peak regions in 22RV1 (NHS and HS) and SM1 (NHS) cells. The promoter regions were defined as regions ±1 kb around transcription start sites. g A Venn diagram showing the genome-wide overlap of HSF1 ChIP-seq peaks identified in 22RV1 cells under HS conditions and SM1 cells under NHS conditions. h A Venn diagram showing the overlap of HSF1-regulated genes (RNA-seq) and HSF1-bound genes (ChIP-seq) in SM1 cells. The heat maps show changes in HSF1 direct target gene expression and HSF1 ChIP-seq signals in SM1 versus SM1-H1KO. i A Venn diagram showing the overlap of HSF1 direct target genes between SM1 and 22RV1 (NHS and HS) cells.