Identification of an NKX3.1-G9a-UTY regulatory network that controls prostate differentiation (Mouse_Recomb_RNA-Seq)
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE81432 | GEO | 2016/06/24
SECONDARY ACCESSION(S): PRJNA321543
REPOSITORIES: GEO
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Project description:Analysis of transcriptome of tissue recombinants (mouse seminal vesicle epithelial [SVE] cells or prostate epithelial [PE] cells, and rat urogenital sinus [UGS] mesenchymal cells) grown under the kidney capsule in athymic nude mice for 3 months. Total RNA obtained from tissue recombinants generated from combining engineered mouse epithelial cells (SVE or PE from 2-month-old C57Bl/6J mice) and rat UGS mesenchymal cells. Tissue recombinants were harvested and processed for RNA isolation and transcriptome analysis using the RNeasy kit (Qiagen).
2016-06-24 | E-GEOD-81432 | biostudies-arrayexpress
Project description:To investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis. This SuperSeries is composed of the SubSeries listed below.
2016-06-24 | GSE81440 | GEO
Project description:To investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-06-24 | E-GEOD-81440 | biostudies-arrayexpress
Project description:Analysis of transcriptome of seminal vesicle from 15-month-old Nkx3.1+/+ mice.
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Project description:Analysis of transcriptome of seminal vesicle from 15-month-old Nkx3.1+/+ mice. Total RNA obtained from seminal vesicle from 15-month-old Nkx3.1+/+ mice. Seminal vesicle was harvested, RNA was extracted using Trizol (Invitrogen, Carlsbad, CA) and purified using an RNeasy kit (Qiagen, Chatsworth, CA). cDNA was labeled using a BioArray High-Yield RNA transcript labeling kit (Enzo Life Sciences, Farmingdale, NY) and hybridized to Affymetrix GeneChips (Mu74AV2).
2016-06-24 | E-GEOD-80600 | biostudies-arrayexpress
Project description:Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is a well-known, ubiquitous estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we first examined the alterations of in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS). Next, to investigate the BPA-specific gene alterations related to increases of the E2 levels and aromatase activity, we performed comprehensive gene expression analysis using Affymetrix GeneChip in the BPA-treated or DES-treated male UGS at embryonic day 17th and postnatal day 1st. Pregnant female C57BL/6 mice were exposed to BPA (20 μg/kg/day) or synthetic estrogen Diethylstilbestrol (DES: 0.2 μg/kg/day), which were dissolved in tocopherol-stripped corn oil, on embryonic day 13 (E13) to E16. Between E17 and postnatal day 1 (P1), all animals were terminated by an overdose of isoflurane followed by cervical dislocation. Fetuses were collected at E17, E18, P0, and P1. The bladder and urethra were removed and dissected to isolate UGS and collected in RNA later. To isolate pure UGS, other tissues such as the bladder, urethra, Wolffian duct (WD), seminal vesicle (SV), and Mullerian duct (MD) were removed from both the male and female urogenital tracts. The histopathology of the mouse UGS was then examined by hematoxylin and eosin staining. Total RNA was extracted using the Qiagen mini RNA Easy kit. Each RNAs were linearly amplified and hybridized to Affymetrix GeneChip.
2010-12-06 | E-GEOD-24928 | biostudies-arrayexpress
Project description:The NKX3.1 homeobox gene plays essential roles in prostate differentiation and prostate cancer. We show that loss of function of Nkx3.1 in mouse prostate results in down-regulation of genes that are essential for prostate differentiation, as well as up-regulation of genes that are not normally expressed in prostate. Conversely, gain of function of Nkx3.1 in an otherwise fully differentiated nonprostatic mouse epithelium (seminal vesicle) is sufficient for respecification to prostate in renal grafts in vivo. In human prostate cells, these activities require the interaction of NKX3.1 with the G9a histone methyltransferase via the homeodomain and are mediated by activation of target genes such as UTY (KDM6c), the male-specific paralog of UTX (KDM6a) We propose that an NKX3.1-G9a-UTY transcriptional regulatory network is essential for prostate differentiation, and we speculate that disruption of such a network predisposes to prostate cancer.
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Project description:Bisphenol A (BPA), an endocrine-disrupting chemical (EDC), is a well-known, ubiquitous estrogenic chemical. To investigate the effects of fetal exposure to low-dose BPA on the development of the prostate, we first examined the alterations of in situ sex steroid hormonal environment in the mouse urogenital sinus (UGS). Next, to investigate the BPA-specific gene alterations related to increases of the E2 levels and aromatase activity, we performed comprehensive gene expression analysis using Affymetrix GeneChip in the BPA-treated or DES-treated male UGS at embryonic day 17th and postnatal day 1st.
2010-12-06 | GSE24928 | GEO
Project description:Cancer cells differentiate along specific lineages that largely determine their clinical and biologic behavior. Distinct cancer phenotypes from different cells and organs likely result from unique gene expression repertoires established during lineage commitment in the embryo and maintained after malignant transformation. We used comprehensive gene expression analysis to examine this concept in the prostate, an organ with a readily manipulable developmental program and a high propensity for cancer. We focused on gene expression changes in the murine prostate rudiment (Urogenital Sinus, UGS) at three time points during the first 48 hours of exposure to androgen, which initiates proliferation and invasion of prostate epithelial buds into surrounding mesenchyme. Keywords: time course, prostate gland development Differential gene expression was assessed by direct comparisons of labeled moieties, using dye-swaps as technical replicates. Hybridizations were performed on the Agilent (Santa Clara, CA) Whole Mouse Genome DNA microarray (mgug4122a). Three different time points were analyzed using RNA pooled from different embryos: • UGS of female embryos upon 6 hours of androgen treatment compared to UGS of vehicletreated mice (H6 comparison, 8 different slides); • UGS of female embryos upon 12 hours of androgen treatment compared to UGS of vehicletreated mice (H12 comparison, 6 different slides); • UGS of male embryos compared to UGS of female embryos (MvsF comparison, 10 different slides). Pools from male tissues were hybridized against pools from female litter-mates;
2008-12-03 | E-GEOD-12077 | biostudies-arrayexpress
Project description:The T-box transcription factor TBX18 is essential to mesenchymal cell differentiation in several tissues and Tbx18 loss-of-function results in dramatic organ malformations and perinatal lethality. Here we demonstrate for the first time that Tbx18 is required for the normal development of periductal smooth muscle stromal cells in prostate, particularly in the anterior lobe, with a clear impact on prostate health in adult mice. Prostate abnormalities are only subtly apparent in Tbx18 mutants at birth; to examine postnatal prostate development we utilized a relatively long-lived hypomorphic mutant and a novel conditional Tbx18 allele. Similar to the ureter, cells that fail to express Tbx18 do not condense normally into smooth muscle cells of the periductal prostatic stroma. However, in contrast to ureter, the periductal stromal cells in mutant prostate assume a hypertrophic, myofibroblastic state and the adjacent epithelium becomes grossly disorganized. To identify molecular events preceding the onset of this pathology, we compared gene expression in the urogenital sinus (UGS), from which the prostate develops, in Tbx18-null and wild type littermates at two embryonic stages. Genes that regulate cell proliferation, smooth muscle differentiation, prostate epithelium development, and inflammatory response were significantly dysregulated in the mutant urogenital sinus around the time that Tbx18 is first expressed in the wild type UGS, suggesting a direct role in regulating those genes. Together, these results argue that Tbx18 is essential to the differentiation and maintenance of the prostate periurethral mesenchyme and that it indirectly regulates epithelial differentiation through control of stromal-epithelial signaling.
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