LncRNA Uc003xsl.1 Activates of NF-?B/IL8 Axis to Promotes Triple-negative Breast Cancer Progression via A Decoy Role to NKRF [ChIP-Seq]

We explore the NF-?B responsive transcription that was regulated by Uc003xsl.1/NKRF complex. The chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) was performed for NKRF in MDA-MB-231-P3 cells treated with si-Uc003xsl.1 or control siRNA. The ChIP-seq data displayed 3604 peak calls in MDA-MB-231-P3 cells against control siRNA and were primarily identified as NF-?B targeting genes. Overall design: The chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) was performed for NKRF in MDA-MB-231-P3 cells treated with si-Uc003xsl.1 or control siRNA.

本研究探究了由Uc003xsl.1/NKRF复合物（Uc003xsl.1/NKRF complex）调控的NF-κB响应性转录。针对经si-Uc003xsl.1或对照小干扰RNA（small interfering RNA, siRNA）处理的MDA-MB-231-P3细胞，我们开展了针对NKRF的染色质免疫共沉淀结合高通量测序（chromatin immunoprecipitation coupled with high-throughput sequencing, ChIP-seq）实验。该ChIP-seq数据在经对照siRNA处理的MDA-MB-231-P3细胞中检出3604个结合峰，且这些峰所关联的基因主要被鉴定为NF-κB靶基因。整体实验设计：针对经si-Uc003xsl.1或对照siRNA处理的MDA-MB-231-P3细胞，开展了针对NKRF的染色质免疫共沉淀结合高通量测序实验。