Defining splicing factor requirements for androgen receptor variant synthesis in advanced prostate cancer

To understand the function of splcing factor MFAP1 in the transcriptional regulation of anrogen receptor variants, we used the CWR22Rv1 prostate cancer cell line depleted of MFAP1 (siMFAP1) or AR-V7 (siCE3) for 72 hours. We then performed gene expression profiling analysis using data obtained from RNA-seq. To investigate the AR-dependent and -independent global transcriptomic impact of MFAP1-depletion using CWR22Rv1 cells depleted of MFAP1 or AR-V7 using siRNA. We then performed gene expression profiling from the RNA sequencing data in response to MFAP1 or AR-V7 depletion compared to the non-targeting scrambled control.

为探究剪接因子MFAP1（splicing factor MFAP1）在雄激素受体变异体（androgen receptor variants）的转录调控中发挥的功能，我们将经小干扰RNA（siRNA）分别敲低MFAP1（siMFAP1）或AR-V7（siCE3）的CWR22Rv1前列腺癌细胞系培养72小时，随后利用RNA测序（RNA-seq）获取的数据开展基因表达谱分析。为进一步探究MFAP1敲低对CWR22Rv1细胞的AR依赖型与非依赖型全局转录组调控效应，我们采用上述经siRNA敲低MFAP1或AR-V7的细胞模型，以非靶向乱序对照（non-targeting scrambled control）为参照，基于RNA测序数据开展基因表达谱分析，以对比MFAP1或AR-V7敲低所引发的转录组变化。