ZBTB7A ChIP-seq under different DHT level

Zinc finger and BTB domain containing transcription repressor ZBTB7A has been recently reported as a tumor suppressor who plays important functions to prevent the progression of prostate cancer. However, the chromatin activity of ZBTB7A in prostate cancer cells remain unclear. In order to identify the cistrome and transcriptome of ZBTB7A, we performed ZBTB7A ChIP-seq in VCaP cells and RNA-seq in VCaP cells transfected with siRNA targeting ZBTB7A or non-targeting control, respectively (cells were grown in full serum). By using combined ChIP-seq and RNA-seq analyses in VCaP cells, we have precisely mapped the ZBTB7A binding sites and identified a subset of genes that are directly repressed by ZBTB7A. To study the chromatin interaction of ZBTB7A with androgen receptor (AR), we also performed ChIP-seq of ZBTB7A in VCaP cells stimulated with 10 nM DHT for 4 hours versus vehicle control (cells were hormone-depleted prior to DHT stimulation). Our results show that ZBTB7A binding is increased by androgen at AR and ZBTB7A overlapping sites. Overall design: First, we performed ChIP-seq analyses to identify ZBTB7A binding sites in VCaP prostate cancer cells, cultured in full serum. Second, we performed RNA-seq analyses to examine genes differentially regulated by ZBTB7A in VCaP cells transfected with siRNA against non-targeting control (siNTC), or ZBTB7A (siZBTB7A), cultured in full serum. Third, we also performed ChIP-seq analyses to identify ZBTB7A chromatin binding under the influence of androgen treatment in VCaP cells treated with or without 10 nM DHT for 4 hours, cultured in hormone-depleted serum. This Series represents the ChIP-seq dataset.