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Links from GEO DataSets

Items: 16

1.
Full record GDS5440

Androgen effect on carboxyl terminal-binding protein 2-deficient prostate cancer cell line

Analysis of androgen receptor (AR)-positive LNCaP prostate cancer cells depleted for carboxyl terminal-binding protein 2 (CTBP2) then treated with the androgen, dihydrotestosterone (DHT). Results provide insight into the molecular effects of CtBP2 knockdown on AR-mediated gene regulation.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 agent, 4 genotype/variation sets
Platform:
GPL6244
Series:
GSE58309
10 Samples
Download data: CEL, CHP
DataSet
Accession:
GDS5440
ID:
5440
2.

Genome wide mapping of AR and its associated factors in prostate cancer

(Submitter supplied) Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and its associated factors such as coregulators or collaborating factors.In addition, by siRNA mediated knockdown of such factors, changes of AR-binding sites in prostate cancer cells were analyzed.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL10999
30 Samples
Download data: BED
Series
Accession:
GSE58428
ID:
200058428
3.

The role of AR-associated factors in androgen signaling

(Submitter supplied) Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified androgen-regulated genes, CTBP2, FOXP1 and RUNX1. These factors interact with AR ligand dependently. In order to investigate androgen-regulated gene functions in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines after siRNA treatment. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5440
Platform:
GPL6244
10 Samples
Download data: CEL, CHP
Series
Accession:
GSE58309
ID:
200058309
4.

Genome wide analysis of AR binding sites and histone modifications in prostate cancer

(Submitter supplied) Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and histone modifications.In addition, by siRNA mediated knockdown of AR-associated factors, changes of AR-binding sites in prostate cancer cells were analyzed..
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL10999
23 Samples
Download data: BAR, TXT
Series
Accession:
GSE62492
ID:
200062492
5.

Effects of RUNX1 knockdown in AR signaling

(Submitter supplied) Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified RUNX1 is an androgen-regulated gene. In order to investigate the RUNX1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines after siRUNX1 treatment. We also treated cells with vehicle or androgen to analyzed the effects of RUNX1 on AR function.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5606
Platform:
GPL6244
4 Samples
Download data: CEL, CHP, TXT
Series
Accession:
GSE62454
ID:
200062454
6.
Full record GDS5606

Androgen effect on runt-related transcription factor 1-deficient prostate cancer cell line

Analysis of androgen receptor (AR)-positive prostate cancer (PC) LNCaP cells depleted for runt-related transcription factor (RUNX1) by siRUNX1 transfection then treated with 10nM dihydrotestosterone (DHT). Results provide insight into the role of RUNX1 in AR-dependent PC.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 2 agent, 2 genotype/variation sets
Platform:
GPL6244
Series:
GSE62454
4 Samples
Download data: CEL, CHP
7.

CHD1 functions as a prostate-specific tumor suppressor by modulating nuclear receptor specificity towards distinct, lineage-specific, enhancers

(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
Series
Accession:
GSE123333
ID:
200123333
8.

Loss of CHD1 facilitates oncogenic hijacking of AR during cancer progression

(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
Series
Accession:
GSE117431
ID:
200117431
9.

CHD1 functions as a prostate-specific tumor suppressor by modulating nuclear receptor specificity towards distinct transcriptional programs [ChIP-seq]

(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
Series
Accession:
GSE117430
ID:
200117430
10.

Loss of CHD1 facilitates oncogenic hijacking of AR during cancer progression [RNA-seq]

(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
Series
Accession:
GSE117429
ID:
200117429
11.

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression after ERG KD)

(Submitter supplied) Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
4 Samples
Download data: TXT
Series
Accession:
GSE35540
ID:
200035540
12.

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression

(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:
GPL9115 GPL10558 GPL6883
27 Samples
Download data: BED, TXT
Series
Accession:
GSE28951
ID:
200028951
13.

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (ChIP-Seq data)

(Submitter supplied) Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
15 Samples
Download data: BED, TXT
Series
Accession:
GSE28950
ID:
200028950
14.

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression data)

(Submitter supplied) Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6883
8 Samples
Download data: TXT
Series
Accession:
GSE28948
ID:
200028948
15.

C-terminal binding protein (CTBP2) is a novel tumor suppressor targeting the MYC-IRF4 axis in multiple myeloma

(Submitter supplied) Multiple myeloma (MM) cells are addicted to MYC and its direct transactivation target IRF4 for proliferation and survival. MYC and IRF4 are still considered “undruggable” as the majority of small molecule inhibitors suffers from low potency, suboptimal pharmacokinetic properties and undesirable off-target effects. Indirect inhibition of MYC/IRF4 emerges as a therapeutic vulnerability in MM. Here, we uncover an unappreciated tumor suppressive role of C-terminal Binding Protein 2 (CTBP2) in MM via strong inhibition of the MYC-IRF4 axis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: TXT
Series
Accession:
GSE255266
ID:
200255266
16.

The effect of Bcl-xL overexpression on H3K3me3

(Submitter supplied) To detect H3K4me3 histone modifications globally in HA-Bcl-xL overexpressing BON1 cells, we performed CUT&RUN assays.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30173
12 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE221629
ID:
200221629
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