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Genome-wide chromatin binding of transcription factor E2F1 in castration resistant prostate cancer (CRPC) cells

ABSTRACT: Our computational approach identified E2F1 as a collaborative factor for EZH2 in transcriptional regulation of cancer-related genes. This experiment is designed to validate the interaction between E2F1 and EZH2 on the chromatin. By obtaining over 1 billion bases of sequence from chromatin immunoprecipitated DNA, we generated the genome-wide localizations of E2F1 in CRPC cell line LNCaP-abl cells, and found that Indeed, these sites are enriched near the transcription start sites of EZH2-activated genes. Further analysis of the transcription factor motifs enriched at these peaks revealed the enrichement of androgen receptor motif, suggesting a co-activator role for EZH2 in concert with AR. Our work demonstrated a novel funtion of EZH2 in transcriptional activation by directly binding to the chromatin sites that cooperate with AR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67809 | GEO | 2015/04/14

SECONDARY ACCESSION(S): PRJNA280968

REPOSITORIES: GEO

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Genome-wide chromatin binding of transcription factor E2F1 in castration resistant prostate cancer (CRPC) cells

Project description:Our computational approach identified E2F1 as a collaborative factor for EZH2 in transcriptional regulation of cancer-related genes. This experiment is designed to validate the interaction between E2F1 and EZH2 on the chromatin. By obtaining over 1 billion bases of sequence from chromatin immunoprecipitated DNA, we generated the genome-wide localizations of E2F1 in CRPC cell line LNCaP-abl cells, and found that Indeed, these sites are enriched near the transcription start sites of EZH2-activated genes. Further analysis of the transcription factor motifs enriched at these peaks revealed the enrichement of androgen receptor motif, suggesting a co-activator role for EZH2 in concert with AR. Our work demonstrated a novel funtion of EZH2 in transcriptional activation by directly binding to the chromatin sites that cooperate with AR. Study of the chromatin localizations of PRC2 complex core subunits and different histone marks in 2 cell types

2015-04-14 | E-GEOD-67809 | biostudies-arrayexpress

Gemone-wide maps of PRC2 complex components and chromatin states in prostate cancer cell lines

Project description:We report the high-throughput profiling of PRC2 core subunits chromatin states and histone modifications in two prostate cancer cell lines, androgen-dependent cells LNCaP and androgen-independent cells LNCaP-abl (abl). By obtaining over 1 billion bases of sequence from chromatin immunoprecipitated DNA, we generated the genome-wide localizations of EZH2, SUZ12 and H3K27 trimethylation in both cell lines, and found that EZH2 can be localized to a subsets of chromating sites that don't have H3K27me3 or SUZ12 signals nearby. Interestingly, these sites are enriched for the active histone marks H3K4 di/trimethylation as well as the RNA polymerase II, which suggest the potential function of these peaks in gene activation. Indeed, these sites are enriched near the transcription start sites of EZH2-activated genes. Further analysis of the transcription factor motifs enriched at these peaks revealed the enrichement of androgen receptor motif, suggesting a co-activator role for EZH2 in concert with AR. Our work demonstrated a novel funtion of EZH2 in transcriptional activation by directly binding to the chromatin sites that cooperate with AR. Study of the chromatin localizations of PRC2 complex core subunits and different histone marks in 2 cell types

2012-11-30 | E-GEOD-39459 | biostudies-arrayexpress

E2F1 transcription factor knockdown effect on gene expression in LNCaP-abl cells

Project description:Our computational approach identified E2F1 as a potential collaborator of EZH2 in androgen-independent prostate cancer. This experiment is to designed to validate the crosstalking of E2F1 and EZH2 pathways. We showed that majority of the EZH2-induced genes in androgen-independent prostate tumor cells are in downstream of E2F1, providing insight into the EZH2-E2F1 collaborative regulatory pathway.

2016-01-22 | GSE56331 | GEO

Genome-wide maps of PRC2 complex components and chromatin states in prostate cancer cell lines

2012-11-30 | GSE39459 | GEO

Hes6 expression is controlled by c-Myc and the AR to promote E2F1 activity and poor outcome in castrate-resistant prostate cancer (E2F1 ChIP-seq)

Project description:Hes6 is a transcription co-factor that is associated with stem cell characteristics in neural tissue, but its role in cancer remains uncertain. Here we show that Hes6 is controlled by c-Myc and the AR and can drive castration resistance in xenografts of the androgen-dependent LNCaP prostate cancer cell line model. Hes6 activates a cell cycle enhancing transcriptional network that maintains tumour growth in the absence of circulating androgen but with maintained nuclear AR. We demonstrate interaction between E2F1, the AR and Hes6 and show the co-dependency of these factors in the castration-resistant setting. In the clinical setting, we have discovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which could be pharmacologically targeted. E2F1 ChIPseq on LNCaP cells.

2014-04-17 | E-GEOD-36614 | biostudies-arrayexpress

EZH2 enables germinal center formation through epigenetic silencing of CDKN1A and an Rb-E2F1 positive feedback loop

Project description:The EZH2 histone methyltransferase is required for B cells to form germinal centers (GCs). Here we show that EZH2 mediates GC formation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21Cip1). Deletion of Cdkn1a rescued the GC reaction in Ezh2 knockout mice. To study the effects of EZH2 in primary GC B cells we generated and validated a 3D B cell follicular organoid system that mimics the endogenous GC reaction. Using this system we found that depletion of EZH2 suppressed G1 to S phase transition of GC B cells in a Cdkn1a dependent manner. GC B cells of Cdkn1a;Ezh2 double knockout mice exhibited high levels of phospho Rb, indicating that loss of Cdkn1a allows progression of cell cycle. Moreover, we show that the transcription factor E2F1 plays a major role in inducing EZH2 upregulation during the GC reaction. E2F1 deficient mice manifest impaired GC responses, which was rescued by restoring EZH2 expression, thus defining a positive feedback loop whereby EZH2 controls GC B cell proliferation by suppressing CDKN1A, allowing cell cycle progression with a concomitant phosphorylation of Rb and release of E2F1.

2017-08-10 | GSE95491 | GEO

E2F1 binding sites in MCF7 cells ENCODE

Project description:E2F1 binding sites in MCF7 cells were determined in the ENCODE regions Keywords: ChIP-chip

2006-03-09 | GSE4355 | GEO

E2F1 ChIP-Seq on mouse hepatocytes overexpressing E2F1

Project description:E2F transcription factors are known regulators of the cell cycle, proliferation, apoptosis and differentiation. We reveal an essential role for E2F1 in liver through the regulation of glycolysis and lipogenesis. E2F1 deficiency leads to a decreased in glycolysis and de novo synthesis of fatty acids in hepatocytes. ChIP-Seq was performed to determine direct tagets of E2F1 in hepatocytes. We highlight that E2F1 directly binds the promoters of genes implicated in metabolic process and notably key lipogenic genes to control these pathways.

2015-12-01 | GSE74006 | GEO

Characterization of an E2f1 acetylation-deficient knock-in mouse model by RNA-Seq profiling

Project description:Objective: The E2F1 transcription factor regulates the expression of genes involved in cell proliferation, apoptosis and other cellular processes. In addition to regulating transcription, a number of studies have revealed novel, transcription-independent functions for E2F1 in regulating DNA repair. E2F1 localizes to sites of DNA damage dependent on its phosphorylation at serine 31 (serine 29 in mice) by the ATM or ATR kinases. In addition to phosphorylation, E2F1 is also acetylated in response to DNA damage on three lysine residues (K117, K120, and K125 in human E2F1), however how acetylation regulates the DNA repair function of E2F1 is unknown. To study the functional significance of E2F1 acetylation in DNA repair in vivo, we generated a targeted mutant mouse line in which the three sites of E2F1 acetylation were mutated from lysine to arginine and named this allele E2f1 3KR. RNA-seq analysis was performed on wild type and E2f1 3KR mouse embryonic fibroblasts (MEFs), before and after treatment with the radiomimetic drug neocarzinostatin (NCS), to examine the impact of the 3KR mutation on global gene expression patterns.

2019-08-05 | GSE135360 | GEO

Hes6 drives a critical AR transcriptional program to induce castration resistant prostate cancer through activation of an E2F1-mediated cell cycle network

Project description:Castrate-resistant prostate cancer (CRPC) is poorly characterized and heterogeneous and while the androgen receptor (AR) is of singular importance, other factors such as c-Myc and the E2F family also play a role in later stage disease. Here we show that Hes6 is up-regulated in aggressive human prostate cancer and drives castration-resistant tumour growth in the absence of ligand binding by enhancing the transcriptional activity of the AR, which is preferentially directed to a regulatory network enriched for other transcription factors including E2F1. In the clinical setting, we have uncovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which can be pharmacologically targeted with restoration of sensitivity to castration. AR and E2F1 ChIPseq from multiple simultaneous LNCaP cell replicates with and without bicalutamide

2014-04-17 | E-GEOD-49832 | biostudies-arrayexpress

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