Elevating PLK1 Overcomes BETi-Resistance in Prostate Cancer via Triggering BRD4 Phosphorylation-dependent Degradation in Mitosis [ChIP-seq]

To investigate the effect of phosphorylated BRD4 at S24 and S1100 on transcription, we established C4-2 stable expressing BRD4 WT, S24/1100A, S24/1100D cell lines in which endogenous BRD4 has been knocked down by shRNA targeted to 3'-UTR. We then performed a CUT&RUN assay using anti-BRD4 or anti-H3K27Ac antibodies followed with a sequencing of ChIPed DNA from 4 different cells at 18 hour treatment of nocodazole. Examination of BRD4 and H3K27Ac modification in human prostate cancer cells C4-2 cells expressing BRD4-WT, -S2A and -S2D mutants. There are 14 ChIP-Seq samples.

为探究S24与S1100位点磷酸化的BRD4对转录的影响，我们构建了内源性BRD4经靶向3'-UTR的短发夹RNA（shRNA）敲除的C4-2细胞系，并在该细胞系中稳定表达BRD4野生型（WT）、S24/1100A及S24/1100D突变体。随后，我们采用抗BRD4抗体或抗H3K27Ac抗体开展CUT&RUN实验，并对经诺考达唑处理18小时的4组细胞的染色质免疫沉淀捕获DNA进行测序。本研究对表达BRD4野生型、S2A及S2D突变体的人前列腺癌C4-2细胞中的BRD4与H3K27Ac修饰进行了检测。本数据集共包含14个ChIP-Seq样本。