E-MTAB-5121
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5121 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-5121-analysis-methods.tsv | Tabular | |||
| E-MTAB-5121-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-5121-configuration.xml | Xml | |||
| E-MTAB-5121-percentile-ranks.tsv | Tabular | |||
| E-MTAB-5121.condensed-sdrf.tsv | Tabular |
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Project description:GATA2 and FOXA1 are pioneering factors for Androgen Receptor (AR) in prostate cancer cells. Less is known about their role in benign epithelial prostate cells. We investigated if they had the ability to induce differentiation in an undifferentiated prostatic context. Benign basal-like prostate epithelial cells 957E/hTERT-AR cells (a gift from John T. Isaacs lab, Johns Hopkins, MD, USA) were transduced with LentiORF RFP control lentiviral particles. The 957E/hTERT-AR-RFP cells were then transduced with GATA2 and FOXA1 lentiviral particles, and we called the new cell lines hTERT/AR-GATA2 and hTERT/AR-FOXA1, respectively. hTERT/AR-GATA2 is a stable selected cell line and treated with 1 nM anabolic steroids, R1881, or ethanol (ET-OH) for 48 hrs. 957E/hTERT/AR-FOXA1 is a transient cell line, because FOXA1 protein is quickly lost. Twenty four hours post transduction with FOXA1 lentivral particles, 1 nM androgen R1881 or ethanol (ET-OH) were added at time for medium exchange and further treated for 24 hours. GATA-2 and FOXA1 ability to induce differentiation was assessed.
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Project description:Analysis of growth factor influence on immortalized human meibomian gland epithelial cells at gene expression level. Growth factors play a critical role in the proliferation and differentiation of sebaceous gland epithelial cells. Given that the meibomian gland is a large sebaceous gland, we hypothesize that growth factors exert analogous effects on human meibomian gland epithelial cells. Results provide important information of the response of human meibomian gland epithelial cells to epidermal growth factor (EGF), bovine pituitary extract (BPE), and both, such as up- or down- regulated genes involved in lipid metabolic process and cell cycle. Human meibomian gland epithelial cells were immortalized in our lab with a retrovirus containing telomerase reverse transcriptase (hTERT). hTERT immortalized cells (3 wells /condition / experiment) were seeded onto 6-well plates at the density of 3.76M-CM-^W104cells /well in SFM basal medium, SFM basal medium with epidermal growth factor (EGF; 5 ng/ml), SFM basal medium with bovine pituitary extract (BPE; 50 M-BM-5g/ml), and SFM basal medium with 5ng/ml EGF plus 50 M-BM-5g/ml BPE (KGM). Total RNA was extracted from cultures in SFM basal medium at day 2, and from cultures in SFM basal medium with BPE, basal medium with EGF, and SFM basal medium with EGF plus BPE at day 7.
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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 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
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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. ChIP-Seq examination of AR and FoxA1 binding sites, FAIRE-seq detection of open chromatin genomic regions in DU145 AR +/- FOXA1 cells
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