Effects of PSF and CTBP1-AS knockdown in prostate cancer cell lines

Prostate cancer is the most common cancer in men and Androgen receptor (AR) downstream signalings promote prostate cancer cell proliferation. We identified androgen-regulated long non-coding RNA, CTBP1-AS, located in the antisese region of CTBP1 gene. CTBP1-AS activate AR signaling by epigenetically repress AR-associated cofactors such as CTBP1 by interactign with RNA-binding protein PSF and recruiting HDAC complex to the target promoters. In order to investigate the CTBP1-AS and PSF function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines after siPSF or siCTBP1-AS treatment. We also treated cells with vehicle or androgen to analyzed the effects of CTBP1-AS and PSF on AR function. Observation of androgen dependent gene expression changes after treatmet with siRNAs targeting CTBP1-AS and PSF with microarray.

前列腺癌是男性最常见的恶性肿瘤，雄激素受体（Androgen receptor, AR）下游信号通路可促进前列腺癌细胞增殖。我们鉴定出一种受雄激素调控的长链非编码RNA（long non-coding RNA）CTBP1-AS，其定位于CTBP1基因的反义区域。CTBP1-AS可通过与RNA结合蛋白PSF结合，并招募组蛋白去乙酰化酶复合物（HDAC complex）至靶基因启动子区域，表观遗传抑制AR相关辅因子（如CTBP1），从而激活AR信号通路。为探究CTBP1-AS与PSF在前列腺癌细胞中的功能，我们在AR阳性前列腺癌细胞系中分别转染靶向PSF或CTBP1-AS的小干扰RNA（siPSF或siCTBP1-AS）后开展基因表达分析。此外，我们还使用溶媒对照或雄激素处理细胞，以分析CTBP1-AS与PSF对AR功能的影响。我们通过基因芯片（microarray）检测了靶向CTBP1-AS与PSF的小干扰RNA处理后，细胞出现的雄激素依赖型基因表达变化。