Transcription factors enriched in tumor-associated enhancers in VHL-deficient ccRCC

VHL loss is the most common genetic alteration event in ccRCC. We profiled histone modifications from VHL-deficient ccRCC primary tumors and cell lines. We show that ccRCCs exhibit a pervasive gain of enhancers around hypoxic and metabolic transcriptional targets. Motif analysis using HOMER revealed significant enrichment of AP-1, ETS, NFĸB and HIFα in tumor enhancers. We generated ChIP-seq binding data for c-Jun, ETS1, NFĸB, and P300, a histone acetyltransferase, in 786-O cells. ChIP-seq profiles of HIF2α and HIF1β in 786-O were already generated previously (GSE34871) Transcription factor ChIP-Seq in ccRCC cell lines

VHL缺失是肾透明细胞癌（ccRCC）最常见的遗传改变事件。本研究对VHL缺陷型肾透明细胞癌原发肿瘤及细胞系的组蛋白修饰进行了全景分析。研究表明，肾透明细胞癌在缺氧应答与代谢相关转录靶点区域的增强子存在广泛扩增。采用HOMER工具开展基序分析显示，肿瘤增强子中显著富集AP-1、ETS、NF-κB及HIFα家族转录因子。本研究在786-O细胞中获取了c-Jun、ETS1、NF-κB以及组蛋白乙酰转移酶P300的染色质免疫共沉淀测序（ChIP-seq）结合数据。此前已有研究生成了786-O细胞中HIF2α与HIF1β的ChIP-seq图谱（GSE34871）。肾透明细胞癌细胞系转录因子ChIP-seq数据集