GEO DataSets

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing

Platforms:

GPL30172 GPL21103 GPL19057

78 Samples

Download data: BED, BW, NARROWPEAK

(Submitter supplied) To define the epigenomic response to AR activation, we employed the 3D organoid model of murine prostate tissue. Control and SPOP-mutant prostate organoids were stimulated with 10 nM dihydrotestosterone (DHT) or vehicle. Next, we performed the transcriptomic analysis (mRNA-seq) together with profiling of the accessibility landscape (ATAC-seq), transcription factor (AR, and FOXA1) binding and H3K4me2 modified nucleosomes.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: CSV

(Submitter supplied) To define the epigenomic response to AR activation, we employed the 3D organoid model of murine prostate tissue. Control and SPOP-mutant prostate organoids were stimulated with 10 nM dihydrotestosterone (DHT) or vehicle. Next, we performed the transcriptomic analysis (mRNA-seq) together with profiling of the accessibility landscape (ATAC-seq), transcription factor (AR, and FOXA1) binding and H3K4me2 modified nucleosomes.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL21103 GPL30172

22 Samples

Download data: BW, NARROWPEAK

(Submitter supplied) To define the epigenomic response to AR activation, we employed the 3D organoid model of murine prostate tissue. Control and SPOP-mutant prostate organoids were stimulated with 10 nM dihydrotestosterone (DHT) or vehicle. Next, we performed the transcriptomic analysis (mRNA-seq) together with profiling of the accessibility landscape (ATAC-seq), transcription factor (AR, and FOXA1) binding and H3K4me2 modified nucleosomes.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL21103

40 Samples

Download data: BED, BIGWIG, NARROWPEAK

(Submitter supplied) To provide further insight to the signaling pathways deregulated by SPOP mutation and determine the relevance of these models to human prostate cancer, we performed RNA-seq on SPOP mutant organoids and controls. RNA-seq reads mapped to human and mouse SPOP confirmed appropriate expression of the F133V transgenic transcript without overexpression compared to endogenous mouse Spop. Quantification of gene expression was performed via RSEQtools using GENCODE as reference gene–annotation set. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

12 Samples

Download data: TXT

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL21103 GPL19057

70 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

4 Samples

Download data: CLOUPE

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

16 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

9 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

9 Samples

Download data: BW

(Submitter supplied) We report the effects of ERG on prostate tumorigenesis, ERG-mediated oncogene addiction, and downstream AR signaling pathways. We determined that ERG facilitates AR-signaling and mediates transformation of prostate cells by maintaining coregulator complex formation at AR-bound sites across the genome.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

8 Samples

Download data: BW

(Submitter supplied) Deregulation of chromatin architecture is emerging as a critical feature of carcinogenesis, and genomic alterations in nucleosome remodelers are common in human cancer. Recurrent deletion of the chromatin remodeler CHD1 is among the most common alterations in prostate cancer, but its role as a tumor suppressor and the reasons for the tissue-specific nature of CHD1 deletion remain undefined. Here, we show that deletion of CHD1 drives prostate tumorigenesis and fundamentally reprograms the transcriptional program of the androgen receptor (AR), diverting AR towards an oncogenic transcriptional program and away from a growth suppressive transcriptome. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL16791

8 Samples

Download data: BED

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL16791 GPL20301 GPL17021

40 Samples

Download data: TXT

(Submitter supplied) Deregulation of chromatin architecture is emerging as a critical feature of carcinogenesis, and genomic alterations in nucleosome remodelers are common in human cancer. Recurrent deletion of the chromatin remodeler CHD1 is among the most common alterations in prostate cancer, but its role as a tumor suppressor and the reasons for the tissue-specific nature of CHD1 deletion remain undefined. Here, we show that deletion of CHD1 drives prostate tumorigenesis and fundamentally reprograms the transcriptional program of the androgen receptor (AR), diverting AR towards an oncogenic transcriptional program and away from a growth suppressive transcriptome. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL20301 GPL16791

16 Samples

Download data: BED

(Submitter supplied) Deregulation of chromatin architecture is emerging as a critical feature of carcinogenesis, and genomic alterations in nucleosome remodelers are common in human cancer. Recurrent deletion of the chromatin remodeler CHD1 is among the most common alterations in prostate cancer, but its role as a tumor suppressor and the reasons for the tissue-specific nature of CHD1 deletion remain undefined. Here, we show that deletion of CHD1 drives prostate tumorigenesis and fundamentally reprograms the transcriptional program of the androgen receptor (AR), diverting AR towards an oncogenic transcriptional program and away from a growth suppressive transcriptome. more...

Organism:

Mus musculus; Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL16791 GPL17021

24 Samples

Download data: TXT

(Submitter supplied) Crosstalk of androgen signaling induced with dihydrotestosterone (DHT) and proinflammatory signaling induced with tumor necrosis-factor alpha (TNFa) was analyzed in prostate cancer cells (LNCaP) by following chromatin binding of androgen receptor (AR), p65 (activating subunit of nuclear-factor kappa-B [NFkB]), FOXA1 and PIAS1+2 chromatin binding using ChIP-seq and transcriptional changes using GRO-seq.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing

Platform:

GPL11154

46 Samples

Download data: BED, TDF

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11154 GPL10558

15 Samples

Download data: BEDGRAPH, CSV, XLSX

(Submitter supplied) Whether the nuclear fraction of mTOR plays a role in prostate cancer (PCa) and can participate in direct transcriptional crosstalk with the androgen receptor (AR) is as yet unknown. The intersection of gene expression, DNA binding-events, and metabolic studies uncovered the existence of a nuclear mTOR-AR transcriptional axis dictating the metabolic rewiring and nutrient usage of PCa cells. In human clinical specimens, nuclear localization of mTOR was significantly associated with metastasis and castration-resistant PCa (CRPC), correlating with a sustained metabolic gene program governed by mTOR in that context. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

3 Samples

Download data: BEDGRAPH, CSV, XLSX