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.含锌指结构域与BTB结构域的转录抑制因子ZBTB7A近期被报道为肿瘤抑制因子，在抑制前列腺癌进展过程中发挥关键功能。然而，ZBTB7A在前列腺癌细胞中的染色质调控活性仍不明确。为鉴定ZBTB7A的顺式调控组（cistrome）与转录组（transcriptome），我们分别在全血清培养的VCaP细胞中开展ZBTB7A染色质免疫共沉淀测序（ChIP-seq），以及在转染靶向ZBTB7A的小干扰RNA（siRNA）或非靶向对照siRNA的VCaP细胞中开展RNA测序（RNA-seq）（细胞均培养于全血清培养基中）。通过联合分析VCaP细胞中的ChIP-seq与RNA-seq数据，我们精准定位了ZBTB7A的结合位点，并筛选出一批受ZBTB7A直接抑制的靶基因。为探究ZBTB7A与雄激素受体（androgen receptor, AR）的染色质互作机制，我们还在经激素剥夺预处理的VCaP细胞中，分别以10 nM双氢睾酮（dihydrotestosterone, DHT）刺激4小时及以溶剂作为对照，开展ZBTB7A的ChIP-seq实验。实验结果表明，雄激素可增强ZBTB7A在AR与ZBTB7A共结合位点处的结合能力。实验整体设计如下：其一，在全血清培养的VCaP前列腺癌细胞中开展ChIP-seq分析，以鉴定ZBTB7A的结合位点；其二，在全血清培养的、转染非靶向对照siRNA（siNTC）或靶向ZBTB7A的siRNA（siZBTB7A）的VCaP细胞中开展RNA-seq分析，以检测受ZBTB7A差异调控的基因；其三，在经激素剥夺培养的VCaP细胞中，分别施加或不施加10 nM DHT刺激4小时，开展ChIP-seq分析，以鉴定雄激素处理条件下ZBTB7A的染色质结合特征。本数据集对应上述ChIP-seq相关的数据系列。