Vitamin D receptor ChIP-Seq in primary prostate epithelial cells
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ABSTRACT:
PROVIDER: PRJNA512526 | ENA |
REPOSITORIES: ENA
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Project description:We investigated the genomic activity of vitamin D in primary prostate epithelial cells (PrE) through vitamin D receptor (VDR)-ChIP-sequencing. PrE cells treated with 50 nM 1,25D showed nuclear localization the VDR within 1 hr, persisting until 4 hr, and a 2 hr treatment was selected for ChIP-seq. Rigorous testing of the ChIP conditions and VDR antibody were performed. Nearly 5,000 VDR binding sites were identified.
2019-04-01 | GSE124576 | GEO
Project description:85 radical prostatectomy specimens (where 16 samples are in Placebo group (PL), 15 are in Selenium group (SE), 25 are in Vitamin E group (VE) and 27 are in Vitamin E & Selenium group (VS.Treatment groups: l-selenomethionine, 400 ug + placebo (vitamin E); vitamin E, 400 IU + placebo (l-selenomethionine); l-selenomethionine, 400 ug + vitamin E, 400 IU; placebos) were subjected to laser capture microdissection to isolate prostate cancer cells, normal epithelial prostatic cells, or stroma cells. RNA extraction and amplification were performed. Transcription profiling was conducted using the HG-U133A Affymetrix arrays.
2008-07-01 | E-MEXP-1327 | biostudies-arrayexpress
Project description:Vitamin D, a hormone that acts through the nuclear vitamin D receptor (VDR), upregulates anti-tumorigenic microRNA in prostate epithelium. This may contribute to the lower levels of aggressive prostate cancer (PCa) in patients with high serum vitamin D. Expression of other small non-coding RNAs (ncRNAs) in prostate epithelium and their potential regulation by vitamin D are uncharacterized. Laser capture microdissection (LCM) followed by small-RNA sequencing was used to identify ncRNA in the prostate epithelium of tissues from a vitamin D-supplementation trial. We compared the expression profiles to small-RNA sequencing data from primary prostate epithelial cells and publically-available benign whole prostate. Application of LCM to isolate epithelium promoted sample homogeneity and captured more diversity in ncRNA species. An abundance of PIWI-interacting RNAs (piRNAs) was detected in normal prostate epithelium, which increased under high vitamin D conditions.
2019-04-01 | GSE124589 | GEO
Project description:The primary goal of this study was to assess differences in gene expression between prostate cancer cell lines and normal prostate epithelial and stromal cells in primary culture.
2008-11-01 | GSE12348 | GEO
Project description:The primary goal of this study was to assess differences in gene expression between prostate cancer cell lines and normal prostate epithelial and stromal cells in primary culture. Experiment Overall Design: 9 samples were analyzed with 1 replicate each. Samples included 6 prostate cancer cell lines, 1 normal prostate epithelial cell system in primary culture, and 2 normal prostate stromal cell systems in primary culture.
2008-11-13 | E-GEOD-12348 | biostudies-arrayexpress
Project description:Signaling through the vitamin D receptor (VDR) has been proposed to suppress the development of epithelial cancers, including prostate cancer. We conducted ChIP-seq to identify the VDR binding sites in the genome of the prostate epithelial cell line, RWPE1. This analysis reveals a large number of VDR binding sites in both control cells and in cells treated with 10 nM 1,25 dihydroxyvitamin D3 for 3 hours. These peaks are associated with genes controlling a wide variety of cellular functions.
2019-04-10 | GSE116843 | GEO
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction. Examination of AR, VDR, and FOXA1 binding in LNCaP cells, in biological replicates
2015-08-01 | E-GEOD-64656 | biostudies-arrayexpress
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction. Gene expression profiling in LNCaP cells after 24hr treatment with different nuclear recpetor ligrands, with time-matching control, in triplicates Expression is assayed with Agilent G4112F.
2015-08-01 | E-GEOD-60956 | biostudies-arrayexpress
Project description:Time course data of normoxia- and hypoxia-treated prostate tumor cell lines (DU145, PC3, LNCaP, 22RV1) and primary prostate epithelial cells (four different donors) in three biological replicates.
2011-11-09 | E-TABM-948 | biostudies-arrayexpress
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction.
2015-08-01 | GSE60956 | GEO