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Links from GEO DataSets

Items: 20

1.

MAP3K7 loss drives enhanced androgen signaling and independently confers risk of recurrence in prostate cancer with joint loss of CHD1

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL24676
64 Samples
Download data: TDF
Series
Accession:
GSE168671
ID:
200168671
2.

RNA-Seq of 22RV1 human prostate cancer cells with knockdown of MAP3K7 and CHD1

(Submitter supplied) Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a human prostate cell line with knockdown of MAP3K7(TAK1) and CHD1, in the presence and absence of androgens. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of deletions of both MAP3K7 and CHD1 in human patients. RNAseq comparing shControl and shMAP3K7/shCHD1 was used to identify transcriptome changes resulting from loss of these genes, as well as their effects on androgen signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
3.

RNA-Seq of LAPC4 human prostate cancer cells with knockdown of MAP3K7 and CHD1

(Submitter supplied) Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a human prostate cell line with knockdown of MAP3K7(TAK1) and CHD1, in the presence and absence of androgens. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of deletions of both MAP3K7 and CHD1 in human patients. RNAseq comparing shControl and shMAP3K7/shCHD1 was used to identify transcriptome changes resulting from loss of these genes, as well as their effects on androgen signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
4.

RNA-Seq of LNCaP human prostate cancer cells with knockdown of MAP3K7 and/or CHD1

(Submitter supplied) Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a human prostate cell line with knockdown of MAP3K7(TAK1) and CHD1, in the presence and absence of androgens. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of deletions of both MAP3K7 and CHD1 in human patients. RNAseq comparing shControl, shMAP3K7(TAK1), shCHD1, and both (shMAP3K7/shCHD1) was used to identify transcriptome changes resulting from loss of each of these genes, as well as their effects on androgen signaling. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: TXT
5.

ChIP-seq of the androgen receptor (AR) in LNCaP human prostate cancer cells with knockdown of MAP3K7 and/or CHD1

(Submitter supplied) Purpose: The goal of this study is to identify genome-wide changes in AR chromatin binding that occur in a human prostate cell line with knockdown of MAP3K7(TAK1) and CHD1, in the presence and absence of androgens. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of deletions of both MAP3K7 and CHD1 in human patients. ChIP-seq comparing AR chromatin binding in shControl, shMAP3K7(TAK1), shCHD1, and both (shMAP3K7/shCHD1) was used to identify AR cistrome changes resulting from loss of each of these genes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
16 Samples
Download data: TDF
Series
Accession:
GSE168651
ID:
200168651
6.

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
7.

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 GPL17021 GPL20301
40 Samples
Download data: TXT
Series
Accession:
GSE117431
ID:
200117431
8.

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
9.

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:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
24 Samples
Download data: TXT
Series
Accession:
GSE117429
ID:
200117429
10.

Downregulation of MED12 via siRNA in SPHEROIDS derived from prostate cancer cell lines (3’ tag DGE)

(Submitter supplied) The Mediator complex is a multi-subunit protein that modulates gene expression on a genome-wide scale. MED12 and cyclin-dependent kinase 8 (CDK8) or its paralog CDK19 are components of its kinase module that regulate the proliferation of prostate cancer cells. In this study, we investigated how MED12 and CDK8/19 influence cancer-driven processes in prostate cancer cell lines, focusing on AR activity and enzalutamide resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL34284
16 Samples
Download data: TXT
Series
Accession:
GSE269073
ID:
200269073
11.

Downregulation of MED12 via siRNA in prostate cancer cell lines (3’ tag DGE)

(Submitter supplied) The Mediator complex is a multi-subunit protein that modulates gene expression on a genome-wide scale. MED12 and cyclin-dependent kinase 8 (CDK8) or its paralog CDK19 are components of its kinase module that regulate the proliferation of prostate cancer cells. In this study, we investigated how MED12 and CDK8/19 influence cancer-driven processes in prostate cancer cell lines, focusing on AR activity and enzalutamide resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
21 Samples
Download data: TXT
Series
Accession:
GSE269072
ID:
200269072
12.

Inhibition of CDK8/CDK19 with the small molecule inhibitor SEL120-34A in prostate cancer cell lines (3’ tag DGE)

(Submitter supplied) The Mediator complex is a multi-subunit protein that modulates gene expression on a genome-wide scale. MED12 and cyclin-dependent kinase 8 (CDK8) or its paralog CDK19 are components of its kinase module that regulate the proliferation of prostate cancer cells. In this study, we investigated how MED12 and CDK8/19 influence cancer-driven processes in prostate cancer cell lines, focusing on AR activity and enzalutamide resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL34284
14 Samples
Download data: TXT
Series
Accession:
GSE269071
ID:
200269071
13.

Downregulation of MED12 via siRNA in 22Rv1 prostate cancer cells (full transcriptome)

(Submitter supplied) The Mediator complex is a multi-subunit protein that modulates gene expression on a genome-wide scale. MED12 and cyclin-dependent kinase 8 (CDK8) or its paralog CDK19 are components of its kinase module that regulate the proliferation of prostate cancer cells. In this study, we investigated how MED12 and CDK8/19 influence cancer-driven processes in prostate cancer cell lines, focusing on AR activity and enzalutamide resistance.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE269070
ID:
200269070
14.

RNA-seq control (sgNT) and TLE3KO (sgTLE3) cells treated with 10 uM enzalutamide or vehicle

(Submitter supplied) To investigate the transcriptional consequences of TLE3 loss in the presence/absence of AR inhibitor enzalutamide in prostate cancer cells, the transcriptomes of WT and TLE3KO cells treated with vehicle or enzalutamide (10 uM) were compared. .
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: XLSX
15.

Endogenous Androgen Receptor proteomic profiling reveals genomic subcomplex involved in prostate tumorigenesis

(Submitter supplied) Androgen Receptor (AR) is a key player in prostate cancer development and progression. Here, we applied immunoprecipitation mass spectrometry of endogenous AR in LNCaP cells to identify individual components of the AR transcription complex. In total, 66 known and novel AR interactors were identified in the presence of R1881, which were critically and selectively required in AR-driven prostate cancer cell proliferation. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
34 Samples
Download data: TXT
Series
Accession:
GSE94682
ID:
200094682
16.

RNAseq of WFU3 mouse prostate epithelial stem cells with knockdown of Map3k7, Chd1, and both

(Submitter supplied) Purpose: The goal of this study is to identify transcriptome-wide changes that occur in a mouse prostate cell line with knockdown of Map3k7(Tak1) and Chd1. We utilize this cell line as a model of an aggressive prostate cancer subtype consisting of loss of both MAP3K7 and CHD1 in human patients. RNAseq comparing shControl, shMap3k7(Tak1), shChd1, and shDouble (both) was used to identify transcriptome changes resulting from loss of these genes of interest in order to identify potential therapeutic vulnerabilites. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
11 Samples
Download data: TXT
Series
Accession:
GSE132664
ID:
200132664
17.

Expression data from prostate cancer LNCaP-AdtHs cells in response to androgen, ADT, normoxia, or hypoxia

(Submitter supplied) Androgen and hypoxia are two cancer hallmark pathways; both exert biological effects primarily via the regulation of gene expression We used gene expression array to determine the global gene expression changes due to androgen, castration (androgen-free) in normoxia and hypoxia conditions. Microarray assays were performed in the OHSU Gene Profiling Shared Resource
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL15207
12 Samples
Download data: CEL
Series
Accession:
GSE120343
ID:
200120343
18.

LX1 Dual Targets AR Variants and AKR1C3 in Advanced Prostate Cancer Therapy

(Submitter supplied) The development of resistance to current standard-of-care treatments, such as androgen receptor (AR) targeting therapies, remains a major challenge in the management of advanced prostate cancer. There is an urgent need for new therapeutic strategies targeting key resistant drivers such as AR variants like AR-V7 and steroidogenic enzymes such as AKR1C3 to overcome drug resistance and improve outcomes for patients with advanced prostate cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
9 Samples
Download data: TXT
Series
Accession:
GSE271696
ID:
200271696
19.

Transcriptome analysis of Enzalutamide-resistant C4-2B (C4-2B MDVR) cells treated with Indocin.

(Submitter supplied) The overall goal of this study was to identify genes that were differentially-expressed in C4-2B MDVR cells treated with Indocin. C4-2B MDVR were either treated with Indocin (20 uM) or DMSO vehicle control for 3 days, followed by isolation of total cellular RNA. Transcriptome analysis was performed with RNA-Sequencing (RNA-Seq) in order to identify differentially-expressed genes (DEGs) induced by Indocin treatment.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
2 Samples
Download data: TXT
20.

Differential gene expression induced by Enzalutamide in a prostate cancer xenograft

(Submitter supplied) RNA-sequencing data of the prostate cancer xenograft PC346C-DCC-K model. Tumor bearing mice were treated daily with Enzalutamide (N=10, 60mg/kg) or placebo (N=5, vehicle) for a period of 7 days. Tumor were subsequently isolated and snap-frozen. Tumor tissue was lysed and homogenized in QIAzol (ref #79306, Qiagen, Hilden, Germany) using an Ultra-Turrax T25 (Janke & Kunkel, Staufen, Germany). Total RNA was isolated using the miRNA-easy mini kit (ref # 217004, Qiagen), and RNA quality was measured using the Bioanalyzer RNA 6000 Nano assay (ref #5067, Agilent, Santa Clara, California, USA). more...
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL25431
15 Samples
Download data: TXT
Series
Accession:
GSE185587
ID:
200185587
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