Project description: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.
Project description: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.
Project description:Prostate cancer is the most common cancer in men and 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 investigated the PSF target genes, we performed ChIP-seq analysis of PSF binding sites in prostate cancer cell line, LNCaP cells. We identified androgen dependent PSF binding regions in prostate cancer cell genome. We observed PSF bindings around the promoters of androgen repressed genes such as CTBP1, p53 and SMAD3. ChIP-sequence analysis of PSF binding sites in prostate cancer cells
Project description:Prostate cancer is the most common cancer in men and 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 investigated the PSF target genes, we performed ChIP-seq analysis of PSF binding sites in prostate cancer cell line, LNCaP cells. We identified androgen dependent PSF binding regions in prostate cancer cell genome. We observed PSF bindings around the promoters of androgen repressed genes such as CTBP1, p53 and SMAD3.
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed RNA sequence analysis in AR positive prostate cancer cell line, LNCaP. In addition, we used hormone-refractory prostate cancer model cells, Long term androgen deprivation (LTAD) to explore the differences of androgen signaling in prostate cancer progression. We analyzed the role of PSF, CTBP1-AS and COBLL1 which we identified as regulators of androgen signaling.