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GSE70048
Mus musculus
55 Downloadable Samples
Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
2-methoxyestradiol (2ME2) induces mammary gland differentiation through amphiregulin-EGFR mediated signaling: molecular distinctions from the mammary gland of pregnant mice.High levels of 2ME2 are observed in the late stages of pregnancy. We investigated the role of 2ME2 on normal mammary gland development. Large scale gene expression assays were performed using Affymetrix GeneChips in pursuit of detailed molecular basis. (1) Mammary glands of wild type FVB mice administered 75 or 150 mg/kg of 2ME2 (2) Mammary glands of normal FVB/Nj mice (i) at day 16 of pregnancy, (ii) day 2 of lactation (iii) day 30 of post-lactation, and (3) mammary epithelial SCp2 cells after 6, 24 and 48 hours of 10 micromol 2ME2 treatment were examined. In vivo studies revealed that 2ME2 treatment up regulates the expression of amphiregulin. The clue to the role of 2ME2 in differentiation comes from studies in vitro which detected down regulation of inhibitor of differentiation (Id-1) gene and consequent up regulation of amphiregulin. The differentiation of E2 negative SCp2 cells by 2ME2 indicate estradiol independent mechanism. For details, please see our paper in Endocrinology 2006.
Publication Title
2-methoxyestradiol induces mammary gland differentiation through amphiregulin-epithelial growth factor receptor-mediated signaling: molecular distinctions from the mammary gland of pregnant mice.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
Illumina Genome Analyzer
Description
The progression of cancer to metastatic disease is a major cause of death. We identified miR-708 being transcriptionally repressed by polycomb repressor complex (PRC2)-induced H3-K27 trimethylation in metastatic breast cancer. miR-708 targets the endoplasmic reticulum protein neuronatin (Nnat) to decrease intracellular calcium (Ca2+) level, resulting in reduction of activation of ERK and FAK, decreased cell migration, and impaired metastases. Functional complementation experiments with Nnat-3’UTR mutant, which is refractory to suppression by miR-708, rescued cell migration and metastasis defects. In breast cancer patients, miR-708 expression was decreased in lymph node and distal metastases, suggesting a metastasis-suppressive role. Our findings uncover a mechanistic role for miR-708 in metastasis and provide a rationale for developing miR-708 as a therapeutic agent against metastatic breast cancer. Overall design: Sequencing miRNAs from Human breast cancer cells: MCF10A, MCF7, MDA-MB-231, MDA-MB-LM2
Publication Title
Suppression of miRNA-708 by polycomb group promotes metastases by calcium-induced cell migration.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Rattus norvegicus
- 28 Downloadable Samples
- Illumina HiSeq 2500
Description
Methamphetamine (Meth) seeking progressively increases after withdrawal (incubation of Meth craving), but the transcriptional mechanisms that contribute to this incubation are unknown. Here we used RNA-sequencing to analyze transcriptional profiles associated with incubation of Meth craving in central amygdala (CeA) and orbitofrontal cortex (OFC), two brain areas previously implicated in relapse to drug seeking. We trained rats to self-administer either saline (control condition) or Meth (10 days; 9 h/day, 0.1 mg/kg/infusion). Next, we collected brain tissue from CeA and OFC on withdrawal day 2 (when Meth seeking is low and non-incubated) and on day 35 (when Meth seeking is high and incubated), for subsequent RNA-sequencing. In CeA, we identified 10-fold more differentially expressed genes (DEGs) on withdrawal day 35 than day 2. These genes were enriched for several biological processes, including protein ubiquitination and histone methylation. In OFC, we identified many fewer expression changes than in CeA. Interestingly, there were more DEGs on withdrawal day 2 than on day 35. Several genes in OFC showed opposing expression changes on withdrawal day 2 (increase) when compared to withdrawal day 35 (decrease), which was further validated by qPCR. Our analyses highlight the CeA as a key region of transcriptional regulation associated with incubation of Meth seeking. In contrast, transcriptional regulation in OFC may contributes to Meth seeking during early withdrawal. Overall, these findings provide a unique resource of gene expression data for future studies examining transcriptional mechanisms in CeA that mediate Meth seeking after prolonged withdrawal. Overall design: Exp. 1 Genome-wide transcriptional profiling of CeA during incubation of Meth craving We performed intravenous surgeries on two groups of rats (total n=26) and trained them to self-administer either saline (n=12) or Meth (n=14) as described above in 2 independent runs. We performed live decapitation on withdrawal days 2 and 35, and collected CeA tissue for mRNA preparation. We used the extracted mRNA for library preparation and RNA-sequencing. We pooled tissue from two rats as one biological replicate. The number of biological replicates in each group was: Day 2: Saline=3, Meth=4; Day 35: Saline=3, Meth=3. Exp. 2 Genome-wide transcriptional profiling of OFC during incubation of Meth craving As above, two groups of rats (total n=32) were trained to self-administer saline (n=16) or Meth (n=16) in 2 independent runs. We performed live decapitation on withdrawal days 2 and 35, and collected OFC tissue for mRNA preparation. We used the extracted mRNA either for library preparation and RNA-sequencing or for cDNA synthesis and qPCR. We pooled tissue from two rats as one biological replicate. The number of biological replicates in each group was: Day 2: Saline=4, Meth=4; Day 35: Saline=4, Meth=4.
Publication Title
Genome-wide transcriptional profiling of central amygdala and orbitofrontal cortex during incubation of methamphetamine craving.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 19 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
A molecular portrait of gastrointestinal stromal tumors: an integrative analysis of gene expression profiling and high-resolution genomic copy number.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 19 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In addition to KIT and PDGFRA mutations, sequential accumulation of other genetic events is involved in the development and progression of gastrointestinal stromal tumors (GISTs). Until recently, the significance of these other alterations has not been thoroughly investigated. The combination of gene expression profiling and high-resolution genomic copy number analysis offers a detailed molecular portrait of GISTs, providing an essential comprehensive knowledge necessary to guide the discovery of novel target genes involved in tumor development and progression.
Publication Title
A molecular portrait of gastrointestinal stromal tumors: an integrative analysis of gene expression profiling and high-resolution genomic copy number.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
Solid tumors are less oxygenated than normal tissues, and for this reason the cancer cells have developed several molecular mechanisms of adaptation to hypoxic environment. Moreover, his poor oxygenation is a major indicator of an adverse prognosis and leads resistance to standard anticancer treatment. Previous reports from this laboratory showed an involvement of Che-1/AATF (Che-1) in cancer cell survival under stress conditions, and on the basis of these observations, we hypothesized that Che-1 might have a role in the response of cancer cells to hypoxia. Methods: The human colon adenocarcinoma cell line HCT116 depleted or not for Che-1 by siRNA, was subjected to normoxic and hypoxic conditions to perform studies about the role of this protein in metabolic adaptation and cell proliferation. The expression of Che-1 under normoxia or hypoxia was detected using western blot assays; cell metabolism was assessed by NMR spectroscopy and functional assays. Further molecular studies were performed by RNA seq, qRT-PCR and ChIP analysis. Results: In this paper we report that Che-1 expression is required for the adaptation of the cells to hypoxia, playing and important role in metabolic modulation. Indeed, Che-1 depletion impacted on glycolysis by altering the expression of several genes involved in the response to hypoxia by modulating the levels of HIF-1alpha. Conclusions: These data demonstrate a novel player in the regulation of a HIF1alpha in response to hypoxia. We found that the transcriptional down-regulation of a members of E3 ubiquitin ligase family SIAH2 by Che-1, produces a failure in the degradation by the hydroxylase PHD3 with a decrease in HIF-1alpha levels during hypoxia. Overall design: The human colon adenocarcinoma cell line HCT116 depleted or not for Che-1 by siRNA was profiled for mRNA high-troughput sequencing (RNA-seq)
Publication Title
Che-1 sustains hypoxic response of colorectal cancer cells by affecting Hif-1α stabilization.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Che-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. Che-1 emerges as an important adaptor that connects transcriptional regulation, cell-cycle progression, checkpoint control, and apoptosis.
Publication Title
Che-1-induced inhibition of mTOR pathway enables stress-induced autophagy.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 15 Downloadable Samples
- Illumina HiSeq 2500
Description
Gene expression analysis in hLECs treated with gain of function or loss of function of MDK in human melanoma cells. Overall design: Biological triplicates of hLEC treated for 3 days with EGM-2 MV conditioned media of melanoma cells. Cell line SK-Mel-147 KD for MDK (shMDK) and its corresponding control (shCtrl (LoF) and WM164 cell line overexpressing MDK (MDK) or an empty vector (NEG) (GoF) were used to produce the conditioned media.
Publication Title
Whole-body imaging of lymphovascular niches identifies pre-metastatic roles of midkine.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Amygdalar MicroRNA-15a Is Essential for Coping with Chronic Stress.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 6 Downloadable Samples
- Illumina Genome Analyzer II
Description
Saccharomyces cerevisiae cannot metabolize cellobiose in nature. Here, S. cerevisiae was engineered to achieve cellobiose utilization by introducing both a cellodextrin transporter gene (cdt-1) and an intracellular ß-glucosidase gene (gh1-1) from Neurospora crassa. We sequenced mRNA from anaerobic exponential cultures of engineered S. cerevisiae grown on cellobiose or glucose as a single carbon source in biological triplicate. Differences in gene expression between cellobiose and glucose metabolism revealed by RNA deep sequencing indicated that cellobiose metabolism induced mitochondrial activation and reduced amino acid biosynthesis under fermentation conditions. Overall design: mRNA levels in cellobiose-grown and glucose-grown cells of engineered cellobiose-utilizing Saccharomyces cerevisiae were examined by deep sequencing, in triplicate, using Illumina Genome Analyzer-II. We sequenced 3 samples from cellobiose-grown cells and 3 samples from glucose-grown cells and identified differential expressions in the cellobiose versus glucose fermentations by using mRNA levels of glucose-grown cells as a reference.
Publication Title
Leveraging transcription factors to speed cellobiose fermentation by Saccharomyces cerevisiae.
Sample Metadata Fields
Cell line, Subject
View Samples