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Genome-wide occupation of AR, FOXA1, and H3K27AC in LNCaP cells treated with selective PARP2 inhibitor UPF-1069

ABSTRACT: Genome-wide occupation of AR, FOXA1, and H3K27AC in LNCaP cells treated with selective PARP2 inhibitor UPF-1069

PROVIDER: PRJNA471000 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7142060.fastq.gz	Fastqsanger.gz
	SRR7142070.fastq.gz	Fastqsanger.gz
	SRR7142061.fastq.gz	Fastqsanger.gz
	SRR7142071.fastq.gz	Fastqsanger.gz
	SRR7142062.fastq.gz	Fastqsanger.gz

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Genome-wide occupation of AR, FOXA1, and H3K27AC in LNCaP cells treated with selective PARP2 inhibitor UPF-1069

Project description:Androgen receptor (AR) signaling is a key driver of prostate cancer (PCa) growth and progression. Understanding the factors influencing AR-mediated transcription provides new opportunities for therapeutic intervention. We have previously discovered that a genetic variant in one of the DNA repair genes, PARP2, is associated with aggressive PCa. Here, we show that a high expression level of PARP2 in PCa tumors is associated with high Gleason scores and biochemical recurrence using The Cancer Genome Atlas (TCGA) dataset. Functional studies reveal that PARP2 enhances AR-mediated gene expression through interacting with the pioneer factor FOXA1 and facilitating AR recruitment to the enhancer regions genome-wide in PCa cells. Selective targeting of PARP2, but not PARP1, by genetic or pharmacological means blocks interaction between PARP2 and FOXA1, which in turn attenuates AR-mediated transcription and inhibits AR-positive PCa growth. SIGNIFICANCE: Current anti-androgens act through blocking ligand binding or inhibiting androgen synthesis. Selective targeting of PARP2 may provide a novel therapeutic approach for AR inhibition by disruption of FOXA1 function, which may be beneficial to patients, irrespective of their DNA repair defect status and, more importantly, when direct AR-targeted therapies fail.

2019-06-24 | GSE114274 | GEO

Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.

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FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [LNCaP, ChIP-seq]

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells

2014-06-02 | E-GEOD-37345 | biostudies-arrayexpress

HNF4G, AR, FOXA1, H3K4me1, H3K27acetyl binding sites upon knockdown and overexpression of HNF4G in 22Rv1 and LNCaP prostate cancer cells respectively

Project description:HNF4G is a gastrointestinal tissue enriched master transcriptional regulator seen overexpressed in a subset of prostate cancer. Here we have mapped binding sites of HNF4G, AR, Foxa1, H3K4me1, H3K27acetyl upon knockdown and overexpression of HNF4G in in 22Rv1 and LNCaP cells respectively

2017-11-01 | GSE85558 | GEO

FOXA1 ChIP-seq in LNCaP cell line overexpressing WT or mutant FOXA1

Project description:FOXA1 ChIP-seq in LNCaP cell line overexpressing WT or mutant FOXA1

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FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [LNCaP, ChIP-seq]

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Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [ChIP-Seq]

Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. ChIP_Seq examination of AR, FoxA1 and GATA2 binding sites in LNCaP and DU145 cells

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Effect of FOXA1 overexpression in prostate cancer

Project description:FOXA1 is a transcription factor which aids AR function in prostate. There is controversary over the effect of high FOXA1 level has on prostate cancer so we forced the overexpression in the LNCaP prostate cancer cell line. LNCaP prostate cancer cell line was transfected with GFP control plasmid or plasmid containing FOXA1 full length cDNA. The effect on gene expression was assessed by microarray.

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Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated engineered LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression. We performed microarray analysis of these cells. We performed microarray analysis on LNCaP cells with FoxA1 knockdown using shRNA or siRNA, 22RV1 cells with stable FoxA1 knockdown and PC3M cells with FoxA1 stable overexpression

2013-04-05 | E-GEOD-37314 | biostudies-arrayexpress

DHT-AR regulation in LNCaP cells and HOXC9 stably expressed LNCaP cells

Project description:To analyze the regulatory mechanism of DHT in LNCaP cells (WT) and HOXC9 stably expressed LNCaP cells (C9), we analyzed the effects of 10-7M of DHT on LNCaP cells.

2025-07-31 | GSE282335 | GEO

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