MED1 is a transcriptional coactivator for gene-specific activators involved in growth and development, we were interested in identifying MED1 target genes potentially involved in prostate development by cDNA microarray. Med1 was conditional knocked out in mice prostate. We performed cDNA microarray with two sets: (1) RNA isolated from three WT ventral prostates and three MT ventral prostates; (2) RNA isolated from three WT lateral prostates and three MT lateral prostates.
No associated publication
Age, Specimen part
View SamplesTo understand molecular mechanisms underlying the synergy of Rb loss and E2F8 loss, we used gene expression profiling to assess molecular changes in Mx1-Cre-mediated knockout (KO) mice using RNA isolated from sorted Ter119+CD71high Erythroblasts.
Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.
Specimen part
View SamplesTumor associated mutant p53 proteins often gain new functions for tumorigenesis and tumor progression. It has been shown that mutant p53 can transcriptionally regulate a group of genes, which in turn contributes to mutant p53 gain of function. A mutant p53 interacting protein Pontin binds to mutant p53 and promotes its gain of function. This experiment tests whether the interaction of Pontin with mutant p53 regulates the transcriptional activity of mutant p53.
No associated publication
Specimen part, Cell line
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer to assemble a mouse prostate cancer interactome.
Cross-species regulatory network analysis identifies a synergistic interaction between FOXM1 and CENPF that drives prostate cancer malignancy.
Treatment
View SamplesTo 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.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Cell line
View SamplesOvarian granulosa cells play a central role in steroidogenesis, which is critical for female reproduction. Follicle-stimulating hormone (FSH) promotes cAMPmediated signaling to regulate granulosa cell steroidogenesis. We have shown previously that 2, 2-bis-(p-hydroxyphenyl)-1, 1, 1-trichloroethane (HPTE) inhibits FSH- and dibutyryl cAMP-stimulated steroidogenesis, and affects the mRNA levels of steroidogenic pathway enzymes in rat granulosa cells. However, HPTE showed a differential effect in FSH- and cAMP-stimulated cells in that HPTE more completely blocked FSH- when compared to cAMP-driven steroidogenesis. The objective of this study was to analyze the effects of HPTE on global gene expression profiles in untreated granulosa cells and those challenged with FSH or cAMP. Granulosa cells from immature rats were cultured with 0, 1, 5, or 10 M HPTE in the presence and absence of either 3 ng FSH/ml or 1 mM cAMP for 48 h. Total RNA was isolated for microarray analysis using the GeneChip Rat Genome 230 2.0 and ArrayAssist Microarray Suite. An investigation of changes in gene expression across all HPTE treatments showed that HPTE altered more genes in FSH- (~670 genes) than in cAMP-stimulated cells (~366 genes). Analysis confirmed that HPTE more effectively inhibited FSH- than cAMP-induced steroid pathway gene expression and steroidogenesis. Furthermore, expression patterns of novel genes regulating signal transduction, transport, cell cycle, adhesion, differentiation, motility and growth, apoptosis, development, and metabolism were all altered by HPTE. This study further established that HPTE exerts differential effects within the granulosa cell steroidogenic pathway, and revealed that these effects include broader changes in gene expression.
Effect of the methoxychlor metabolite HPTE on the rat ovarian granulosa cell transcriptome in vitro.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Disease, Disease stage, Treatment
View SamplesThe estimation of acceptable exposure levels for genotoxicants is accomplished by defining thresholds from apical endpoints, or by modeling points of departure from data that are acquired from high dose experiments, followed by linear extrapolation of the response through zero. We recently proposed that low dose exposure-induced transcriptional changes that can be linked to mechanisms of pathogenesis could provide a more sensitive alternative for defining thresholds for biological responses. In the present study, we used gene expression profiling data to determine an empirical transcriptional dose response threshold for the food and tobacco smoke borne carcinogen, 2-amino-1-methyl-6-phenylimidazo[4,5]pyridine (PhIP) in human BEAS-2B bronchial epithelial cells exposed to concentrations of N-hydroxylated PhIP ranging from 1 x 10-6 to 5 x 10-10 M.
No associated publication
Cell line, Treatment
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Treatment
View SamplesMultiple Sclerosis (MS) is an immune-mediated chronic inflammatory disease affecting the central nervous system. The cause of MS is not known and the mechanism of IFN-beta, a disease-modifying treatment (DMT) approved for MS, is not well-understood. Oligonucleotide microarrays were used to study gene expression in plasmacytoid denditic cells (pDCs) which are antigen-presenting cells implicated in MS pathogenesis.
Multiple sclerosis-linked and interferon-beta-regulated gene expression in plasmacytoid dendritic cells.
Sex, Age, Specimen part, Disease, Disease stage, Subject
View Samples