Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA213143 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR941936.fastq.gz | Fastqsanger.gz | |||
| SRR941937.fastq.gz | Fastqsanger.gz | |||
| SRR941938.fastq.gz | Fastqsanger.gz | |||
| SRR941939.fastq.gz | Fastqsanger.gz | |||
| SRR941940.fastq.gz | Fastqsanger.gz |
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Project description:The ETS family member GABPa mediates the development of castrate-resistant prostate cancer (BeadChip)
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Project description:In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABPá, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes. VCaP prostate cancer cells and Jurkat lymphoma cells were studied for the ETS factors ERG and GABPa binding sites. Each sample was compared to its input.
2014-05-21 | E-GEOD-49091 | biostudies-arrayexpress
Project description:In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABPá, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes. Cells were made to either overexpress GABPa or have it knocked down; these conditions also had empty vector and non-targetting controls respectively. All four treatments were carried out with and without androgen for the LNCaP and c42b cell lines. Biological and technical replicates were used.
2014-05-21 | E-GEOD-49083 | biostudies-arrayexpress
Project description:The ETS transcription factor GABPA controls cell migration in breast epithelial cells through targeting a cohort of genes, independently from another family member ELK1, and thereby achieves biological specificity. Here, both direct and indirect target genes for GABPA are identified by siRNA silencing of GABPA. Therefore, although ELK1 and GABPA ultimately control the same biological process, they do so by regulating distinct cohorts of target genes associated with actin cytoskeletal functions and cell migration control.
2013-07-15 | E-MEXP-3682 | biostudies-arrayexpress
Project description:In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABPá, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes.
2014-05-21 | GSE49091 | GEO
Project description:In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABPá, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes.
2014-05-21 | GSE49083 | GEO
Project description:This study aimed to elucidate the role of ELF3, an epithelia-specific member of the ETS family, in normal prostate development and prostate cancer. Four comparisons (untreated, mock-transfected, scrambled siRNA, and targeted siRNA) were performed in two prostate epithelial cell lines BPH-1 (benign) and PC3 (malignant). Global gene expression arrays were performed for each combination.
2022-04-25 | E-MTAB-11485 | biostudies-arrayexpress
Project description:Prostate gland is a highly androgen dependent gland. The first line of treatment for metastatic prostate cancer therefore, is androgen ablation. This can be achieved by multiple non-surgical methods. However, most of these cancers although respond well initially, become resistant to androgen ablation sooner or later. These cancers then become extremely aggressive and difficult to treat, thereby drastically affect the patient prognosis. A gene expression signature for castrate resistant prostate cancer would be useful in identification of mechanisms responsible for castrate resistance, as well as to predict the progression of the cancer into castrate resistance. For this, our group has done a RNA-seq analysis of a. Control group (C); b. Castrate Sensitive group (B) and c. Castrate Resistant group (A). Gene expression profiling was performed on these samples using RNA-seq. Differentially expressed genes between control and castrate sensitive as well as control and castrate resistant groups were identified.
2024-09-11 | GSE262940 | GEO
Project description:A central question in transcription factor biology is how a specific member of a transcription factor family occupies a promoter in vivo, when all family members bind the same consensus site in vitro. To uncover the mechanisms regulating DNA binding specificity within transcription factor families, we have used the techniques of chromatin immunoprecipitation coupled with genome-wide microarray analysis to query the occupancy of three members of the ETS transcription factor family in a human T-cell line. Unexpectedly, redundant occupancy was frequently detected while specific occupancy was less likely. An unbiased bioinformatics approach correlated redundant binding with consensus ETS binding sequences near transcription start sites, whereas specific binding sites diverged dramatically from the consensus, were coupled with a site for a cooperative binding partner, and were found further from transcription start sites. The specific and redundant DNA binding modes illustrate the regulation of transcription factor specificity in vivo and suggest two distinct roles for members of the ETS transcription factor family. Keywords: ChIP-chip Chromatin IP from uninduced asynchronous Jurkat T cells, or HT29 colon cells using antibodies to three ETS transcription factors (ETS1, ELF1, and GABPa) or the transcription factors RUNX1 or E2F4. IP and whole input DNAs are amplified (WGA2 kit sigma) and labeled and compared by promoter microarrays (Agilent). Each experiment requires 2 microarrays to cover the genome. Proximal promoter arrays assay 1kb surrounding transcription start sites, extended promoter arrays assay 7kb surrounding transcription start sites. Each microarray is performed as two biological replicates with the exception of ETS1 in HT29 proximal promoter array which were done once, and ETS1 in Jurkat proximal promoter array which was done three times.
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