Studies of gene expression profiles using the whole genome wide microarray analysis in SUM149PT cells (ER-, p53mut) and SUM190PT cells (ER-, p53mut) when treated with 5 or 7.5 M CG-1521 alone and in combination with 10 nM 17-Estradiol. Comparisons between each treatment group provides evidence for the dysregulation of genes associated with the spindle assembly checkpoint.
Histone deacetylase inhibitors modulate miRNA and mRNA expression, block metaphase, and induce apoptosis in inflammatory breast cancer cells.
Cell line
View SamplesCrosstalk between Aryl hydrocarbonreceptor (AHR) and Estrogen receptor (ER) is poorly understood, but seems to play a major role in female reproductive organs.
Cross-Talk in the Female Rat Mammary Gland: Influence of Aryl Hydrocarbon Receptor on Estrogen Receptor Signaling.
Sex, Specimen part
View SamplesPurpose: identification of mRNAs that are potential targets of miR-203 in the endometrium and endometrial carcinoma Methods: mRNA profiles of three batches of wild-type (WT) and three independently generated miR-203 knockout (miR-203 KO) RUCA-I cells were produced by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped between 30 and 50 million sequence reads per sample to the rat genome (build rn6) and identified 26751 transcripts of which 1591 are differentially expressed in WT and miR-203 KO cells (p<0.05). Overall design: mRNA profiles of three WT batches and three independently generated miR-203 KO RUCA-I rat endometrial adenocarcinoma cell lines were produced by deep sequencing, using Illumina HiSeq2500.
Role of miR-203 in estrogen receptor-mediated signaling in the rat uterus and endometrial carcinoma.
No sample metadata fields
View SamplesExamination of crosstalk between Aryl hydrocarbonreceptor (AHR) and Estrogen receptor (ER) in the rat uterus on the level of mRNA transcriptome
Effects of the aryl hydrocarbon receptor agonist 3-methylcholanthrene on the 17β-estradiol regulated mRNA transcriptome of the rat uterus.
Sex, Specimen part, Treatment
View SamplesThe goal of this study was to determine how decreased mitochondrial citrate export influences gene expression in Drosophila larvae. RNA was isolated from Drosopohila sea mutants, which exhibiti decreased mitochondrial citrate transport activity, and a genetically-matched control strain during mid-L3 development. Overall design: Larvae were collected as described in Li, H., Tennessen, J. M. Preparation of Drosophila Larval Samples for Gas Chromatography-Mass Spectrometry (GC-MS)-based Metabolomics. J. Vis. Exp. (136), e57847, doi:10.3791/57847 (2018). RNA was purified from staged mid-L3 larvae using a RNeasy Mini Kit (Qiagen). Sequencing was performed using an Illumina NextSeq500 platform with 75 bp sequencing module generating 41 bp paired-end reads. After the sequencing run, demultiplexing was performed with bcl2fastq v2.20.0.422.
A <i>Drosophila</i> model of combined D-2- and L-2-hydroxyglutaric aciduria reveals a mechanism linking mitochondrial citrate export with oncometabolite accumulation.
Subject
View SamplesCancer cells utilize a unique form of aerobic glycolysis, called the Warburg effect, to efficiently produce the macromolecules required for proliferation. Here we show that a metabolic program related to the Warburg effect is used during normal Drosophila development and regulated by the fly ortholog of the Estrogen-Related Receptor (ERR) family of nuclear receptors. dERR null mutants die as second instar larvae with abnormally low ATP levels, diminished triacylglyceride stores, and elevated levels of circulating sugars. Metabolomic profiling revealed that the pathways affected in these mutants correspond to those used in the Warburg effect. The expression of active dERR protein in mid-embryogenesis triggers a coordinate switch in gene expression that drives a metabolic program supporting the dramatic growth that occurs during larval development. This study suggests that mammalian ERR family members may promote cancer by directing a metabolic state that supports proliferation.
The Drosophila estrogen-related receptor directs a metabolic switch that supports developmental growth.
Specimen part
View SamplesIdentification of transcriptional profiles stimulated by the complement protein C1q in rat immature neurons associated with the C1q-dependent neuroprotection observed in vitro.
Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression.
Specimen part
View SamplesIn this study, we developed a unique system using primary human autologous lymphocytes and HMDMs to characterize the effect of C1q on macrophage gene expression profiles during the uptake of apoptotic cells. Our results showed that C1q bound to autologous apoptotic lymphocytes (AL) significantly modulated the response of HMDMs to LPS by increasing expression of cytokines, chemokines and effector molecules associated with immunoregulation and by directly suppressing caspase-1 dependent cleavage of IL-1beta.
Complement protein C1q directs macrophage polarization and limits inflammasome activity during the uptake of apoptotic cells.
No sample metadata fields
View SamplesPersistent bronchial dysplasia (BD) is associated with increased risk of developing invasive squamous cell carcinoma (SCC) of the lung. We hypothesized that differences in gene expression profiles between persistent and regressive BD would identify cellular processes that underlie progression to SCC. RNA expression arrays (Affymetrix Hu 1.0) comparing baseline biopsies from 32 bronchial sites that persisted/progressed to 31 regressive sites showed 395 differentially expressed genes (ANOVA, FDR</=0.05). Thirty-one pathways showed statistically significant evidence of altered activity between the two groups. Multiple pathways were associated with cell cycle control/proliferation, inflammation, or epithelial differentiation/cell-cell adhesion. Polo-like kinase 1 (PLK1) was associated with multiple cell cycle pathways. Cultured persistent BD cells showed increased PLK1 expression, and following treatment with PLK1 inhibitor, showed induction of apoptosis, G2/M phase arrest and decreased proliferation compared to untreated cells. These effects were not seen in normal or regressive BD cultures. Inflammatory pathway activity was decreased in persistent BD and the presence of an inflammatory infiltrate was more common in regressive BD. Regressive BDs were also associated with trends toward overall increases in macrophages and T-lymphocytes and altered polarization of these inflammatory cell subsets. Increased desmoglein 3 and plakoglobin expression was associated with higher grade and persistence of BD. The results identify alterations in cell cycle control, inflammatory activity, and epithelial differentiation/cell-cell adhesion in the persistent subset of BDs that are associated with high risk for progression to invasive SCC. These pathways may provide strong markers of risk and effective targets for lung cancer prevention.
Altered Cell-Cycle Control, Inflammation, and Adhesion in High-Risk Persistent Bronchial Dysplasia.
Age, Specimen part
View SamplesComplement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection.
C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.
Specimen part, Treatment
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