Distinctive gene expression of prostatic stromal cells cultured from diseased versus normal tissues
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE6250 | GEO | 2006/11/10
SECONDARY ACCESSION(S): PRJNA97525
REPOSITORIES: GEO
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Project description:To obtain a comprehensive view of the transcriptional programs in prostatic stromal cells of different histological/pathological origin, we profiled 18 adult human stromal cell cultures from normal transition zone (TZ), normal peripheral zone (PZ), benign prostatic hyperplasia (BPH), and prostate cancer (CA) using cDNA microarrays.
2006-11-06 | E-SMDB-3867 | biostudies-arrayexpress
Project description:We generated prostatic stromal microarray expression data for functional validation of our LOH/AI hot-/cold-spots in stroma. Stromal cells from normal peripheral zone tissue and from tumors are grown in culture, and were analyed on gene expression platform. Stromal cells cultured from normal peripheral zone tissues (F-PZ-64, F-PZ-79, F-PZ-82, F-PZ-102, F-PZ-105) and from tumors (F-CA-31, F-CA-39, F-CA-52, F-CA-67, F-CA-93) were established and grown as previously described in Peehl et al. (2000). Total RNAs were extracted from semi-confluent cells (passages 4-5) one day after feeding fresh medium using RNeasy Mini Kit (Qiagen) according to the manufacturer’s instructions and treated with TURBO DNA-free kit (Ambion). Hybridizations were performed according to Illumina protocols by the Genomic Core, Lerner Research Institute, Cleveland Clinic. All samples were hybridized to the Illumina Sentrix Human-6_v3 Expression BeadChip (GPL6884) which contains 48,000 distinct oligonucleotide probes. Normalization is done using average normalization algorithm of BeadStudio Gene Expression Module v3.4 (Illumina).
2012-02-27 | E-GEOD-34312 | biostudies-arrayexpress
Project description:The identification of cellular and functional heterogeneity within the prostate and between the transitional zone (TZ) and peripheral zone (PZ) is critical for understanding the spatial distribution of prostate diseases. Three paired human prostate PZ and TZ tissue samples were used for scRNA-seq.
2024-02-13 | GSE166782 | GEO
Project description:To identify the genes differently expressed in the epithelium and the stromal of Benign Prostatic Hyperplasia (BPH), we collect the epithelium and the stromal from the patients with benign prostatic hyperplasia by laser micro-dissection. And then, Affymetrix HG-U133_Plus_2 gene-chip was used to detect and compare the expression level of genes. To find which genes are most abundantly expressed in epithelium and stromal and what is the role of these genes in the pathogenesis of BPH.
2011-08-10 | GSE31323 | GEO
Project description:Induced pluripotent stem (iPS) cells are a valuable resource for discovery of epigenetic changes critical to cell type-specific differentiation. Although iPS cells have been generated from other terminally differentiated cells, the reprogramming of normal adult human basal prostatic epithelial (E-PZ) cells to a pluripotent state has not been reported. Here, we attempted to reprogram E-PZ cells by forced expression of Oct4, Sox2, c-Myc, and Klf4 using lentiviral vectors and obtained embryonic stem cell (ESC)-like colonies at a frequency of 0.01%. These E-PZ-iPS-like cells with normal karyotype gained expression of pluripotent genes typical of iPS cells (Tra-1-81, SSEA-3, Nanog, Sox2, and Oct4) and lost gene expression characteristic of basal prostatic epithelial cells (CK5, CK14, and p63). E-PZ-iPS-like cells demonstrated pluripotency by differentiating into ectodermal, mesodermal, and endodermal cells in vitro, although lack of teratoma formation in vivo and incomplete demethylation of pluripotency genes suggested only partial reprogramming. Importantly, E-PZ-iPS-like cells re-expressed basal epithelial cell markers (CD44, p63, MAO-A) in response to prostate-specific medium in spheroid culture. Androgen induced expression of androgen receptor (AR), and co-culture with rat urogenital sinus further induced expression of prostate-specific antigen, a hallmark of secretory cells, suggesting that E-PZ-iPS-like cells have the capacity to differentiate into prostatic basal and secretory epithelial cells. Finally, when injected into mice, E-PZ-iPS-like cells expressed basal epithelial cell markers including CD44 and p63. When co-injected with rat urogenital mesenchyme, E-PZ-iPS-like cells expressed AR and expression of p63 and CD44 was repressed. DNA methylation profiling identified key pathways and regulators of prostatic differentiation including Wnt5a, BPM7, PTEN, and NKx3.1 using E-PZ-iPS-lke cells. Our results suggest that iPS-like cells can be derived from prostatic epithelial cells. These cells are pluripotent and capable of prostatic differentiation, and therefore provide a novel model for investigating epigenetic changes involved in prostate cell lineage specification.
2016-01-01 | GSE45469 | GEO
Project description:To identify the genes differently expressed in the epithelium and the stromal of Benign Prostatic Hyperplasia (BPH), we collect the epithelium and the stromal from the patients with benign prostatic hyperplasia by laser micro-dissection. And then, Affymetrix HG-U133_Plus_2 gene-chip was used to detect and compare the expression level of genes. To find which genes are most abundantly expressed in epithelium and stromal and what is the role of these genes in the pathogenesis of BPH. 8 prostate tissues were collected from patients undergone transurethral resection of the prostate (TURP) with informed consent. Each tissue was embedded in O.C.T and subsequently used for laser micro-dissection. The total RNA was isolated from each sample and equally mixed for gene-chip assay.
2011-08-09 | E-GEOD-31323 | biostudies-arrayexpress
Project description:Analysis of gene expression in prostatic tissue from BPH patients with and without SRD5A2 gene methylation. The hypothesis is that BPH patients with DNA methylation of the SRD5A2 gene promoter have impaired conversion of testosterone to dihydrotestosterone, and therefore may use an alternative signaling pathway for prostatic tissue growth. Here, we compare gene expression profiles of SRD5A2-methylated vs. unmethylated prostatic tissue to nominate alternative biological pathways relevant in each molecular subtype of BPH.
2017-10-01 | GSE101486 | GEO
Project description:Induced pluripotent stem (iPS) cells are a valuable resource for discovery of epigenetic changes critical to cell type-specific differentiation. Although iPS cells have been generated from other terminally differentiated cells, the reprogramming of normal adult human basal prostatic epithelial (E-PZ) cells to a pluripotent state has not been reported. Here, we attempted to reprogram E-PZ cells by forced expression of Oct4, Sox2, c-Myc, and Klf4 using lentiviral vectors and obtained embryonic stem cell (ESC)-like colonies at a frequency of 0.01%. These E-PZ-iPS-like cells with normal karyotype gained expression of pluripotent genes typical of iPS cells (Tra-1-81, SSEA-3, Nanog, Sox2, and Oct4) and lost gene expression characteristic of basal prostatic epithelial cells (CK5, CK14, and p63). E-PZ-iPS-like cells demonstrated pluripotency by differentiating into ectodermal, mesodermal, and endodermal cells in vitro, although lack of teratoma formation in vivo and incomplete demethylation of pluripotency genes suggested only partial reprogramming. Importantly, E-PZ-iPS-like cells re-expressed basal epithelial cell markers (CD44, p63, MAO-A) in response to prostate-specific medium in spheroid culture. Androgen induced expression of androgen receptor (AR), and co-culture with rat urogenital sinus further induced expression of prostate-specific antigen, a hallmark of secretory cells, suggesting that E-PZ-iPS-like cells have the capacity to differentiate into prostatic basal and secretory epithelial cells. Finally, when injected into mice, E-PZ-iPS-like cells expressed basal epithelial cell markers including CD44 and p63. When co-injected with rat urogenital mesenchyme, E-PZ-iPS-like cells expressed AR and expression of p63 and CD44 was repressed. DNA methylation profiling identified key pathways and regulators of prostatic differentiation including Wnt5a, BPM7, PTEN, and NKx3.1 using E-PZ-iPS-lke cells. Our results suggest that iPS-like cells can be derived from prostatic epithelial cells. These cells are pluripotent and capable of prostatic differentiation, and therefore provide a novel model for investigating epigenetic changes involved in prostate cell lineage specification. Bisulphite converted DNA from the 10 samples were hybridised to the Illumina Infinium HumanMethylation450K Beadchip v1.2
2016-07-03 | E-GEOD-45469 | biostudies-arrayexpress
Project description:We generated prostatic stromal microarray expression data for functional validation of our LOH/AI hot-/cold-spots in stroma. Stromal cells from normal peripheral zone tissue and from tumors are grown in culture, and were analyed on gene expression platform.
2012-02-27 | GSE34312 | GEO
Project description:Benign prostatic hyperplasia (BPH) may decrease patient quality of life and often leads to acute urinary retention and surgical intervention. While effective treatments are available, many BPH patients do not respond or develop resistance to treatment. To understand molecular determinants of BPH treatment resistance, we investigated gene expression profiles before and after treatments in the prostate transitional zone of 108 participants in the Medical Therapy of Prostatic Symptoms (MTOPS) Trial. Unsupervised clustering revealed molecular subgroups characterized by expression changes in a large set of genes associated with resistance to finasteride, a 5α-reductase inhibitor. Pathway analyses within this gene cluster found finasteride administration induced changes in fatty acid metabolism, amino acid metabolism, immune response, steroid hormone metabolism, and kinase activity within the transitional zone. We found that patients without this transcriptional response were highly likely to develop drug resistance, which is expected in 33% of finasteride-treated patients. Importantly, a patient’s transcriptional response to finasteride was associated with their pre-treatment kinase expression. Further, we identified novel expression signatures of finasteride resistance among the transcriptionally responded patients. These patients showed different gene expression profiles at baseline and increased prostate transitional zone volume compared to the patients who responded to the treatment. Our work suggests molecular mechanisms of resistance to finasteride treatment that could be potentially helpful for personalized BPH treatment as well as new drug development to increase patients drug response.
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