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SRP144174
Mus musculus
5 Downloadable Samples
NextSeq 500
Description
Purpose: We tested global gene transcriptome changes by RNA-sequencing analysis in the offspring breast tumors of SV40 transgenic mice to further identify key epigenetic-controlled genes in regulation of the prenatal/maternal BSp diet-mediated early breast cancer prevention. Method: Mouse offspring mammary tumor mRNA from control and maternal BSp treatment were generated by deep sequencing, in duplicate or triplicate, using Illumina NextSeq500 platform (GPL19057). The sequence reads that passed quality filters were analyzed. We utilized the R/Bioconductor package DESeq to evaluate differential gene expression for sequence count data by the use of negative binomial distributio. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Conclusions: Our data showed differential transcriptome distribution in the breast tumors of mouse offspring between the control and prenatal/maternal BSp treatment groups. Overall design: Total RNA obtained from the offspring breast tumors of SV40 transgenic mice with mothers fed either control or BSp diets, and analyzed by Illumina NextSeq500 platform (GPL19057).
Publication Title
Temporal Efficacy of a Sulforaphane-Based Broccoli Sprout Diet in Prevention of Breast Cancer through Modulation of Epigenetic Mechanisms.
Sample Metadata Fields
Age, Cell line, Treatment, Subject
View Samples- Homo sapiens
- 10 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
transcriptome profiling of miR-92a inhibitor treated and control cells with the aim of measuring miR-92a influence on its mRNA targets
Publication Title
Mapping the human miRNA interactome by CLASH reveals frequent noncanonical binding.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
HESC-H9 and iPSC lines 3.5, 3.6 and 3.12 were analyzed using Affymetrix microarray before and after Definitive Endoderm (DE) formation. DE was induced using the ActivinA differentiation protocol described by D'Amour et al., 2006 (PMID: 16258519) Clustering analysis of transcripts that were differentially regulated during DE formation indicated that iPSC lines 3.5 and 3.12 differentiate in manner that is highly similar to HESC-H9 cells iPSC line 3.6 had a more divergent transcriptional profile.
Publication Title
Directed differentiation of human pluripotent stem cells into intestinal tissue in vitro.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 52 Downloadable Samples
- Illumina HumanRef-8 v3.0 expression beadchip
Description
We performed gene expression profiling of 26 colorectal tumors and matched histologically normal adjacent colonic tissue samples using the Illumina Ref-8 whole-genome expression BeadChip. We performed an integrated analysis of promoter DNA methylation and gene expression data to investigate the effects of DNA hypermethylation on gene expression.
Publication Title
Genome-scale analysis of aberrant DNA methylation in colorectal cancer.
Sample Metadata Fields
Sex, Disease, Disease stage
View Samples- Homo sapiens
- 60 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
Actinic keratosis is a common skin disease that may progress to invasive squamous cell carcinoma. Ingenol mebutate has demonstrated efficacy in field treatment of actinic keratosis. However, molecular mechanisms on ingenol mebutate response are not yet fully understood.
Publication Title
Identification of differentially expressed genes in actinic keratosis samples treated with ingenol mebutate gel.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix CytoScan HD Array (cytoscanhdarray), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptome and cytogenetic profiling analysis of matched in situ/invasive cutaneous squamous cell carcinomas from immunocompetent patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Subject
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
Although most cutaneous squamous cell carcinomas (cSCC) develop from actinic keratoses (AK), the key events for this evolution remain unclear. We have combined the results of different genomic and expression array platforms on matched samples of sun-exposed skin, AK and cSCC from ten immunocompetent patients, with the objective of better understanding the mechanisms involved in this progression. Gene expression analysis and copy number alterations were assessed using GeneChip Human Gene 2.0 ST Array (Affymetrix) and CytoScan HD Cytogenetics Solution (Affymetrix) platforms, respectively. Integration of genome and transcriptome results was evaluated using the DR-Integrator tool. Additional studies (qPCR, immunohistochemistry and Western blot) were performed for selected genes. Twenty-two genes showed a progressive expression spectrum from clinically normal sun-exposed skin samples to cSCC. FOSL1 and BNC1 encode transcription factors whose expression was increased in cSCC in the expression array and the qPCR. By immunohistochemistry, FOSL1 showed an intense staining at the invasive front of cSCC samples and BNC1 expression varied from a nuclear location (sun-exposed skin) to a cytoplasmic location (cSCC). Western blot analyses confirmed the enhancement of FOSL1 and BNC1 expression. Additionally, the smallest overlapping regions of genomic imbalance (SORIs) involving at least 3 of the samples of each group (sun-exposed skin, AK or cSCC) were selected. One of the SORIs was a deletion in the p24.1 band of chromosome 3, shared by 7 of the cSCC. A strong correlation in the integration analysis was found for NEK10, a gene contained in the previously mentioned SORI. Loss of NEK10 expression in cSCC was confirmed by immunohistochemistry and western blot analyses. In conclusion, our findings suggest that FOSL1 may play a role in promoting the cSCC invasion ability. We have also identified two additional genes, NEK10 and BNC1, which could also act as tumor drivers.
Publication Title
Transcriptome and cytogenetic profiling analysis of matched in situ/invasive cutaneous squamous cell carcinomas from immunocompetent patients.
Sample Metadata Fields
Sex, Age, Specimen part, Disease stage, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2000
Description
The goal of the study was to understand how integrin beta1 expressed in epithelial cells directs developmental angiogenesis. Integrin beta1 was deleted specifically in the pituitary glands of embryonic mice. RNA was isolated from knockout and WT control pituitaries dissected at e12.5, one day prior to the initiation of developmental angiogenesis. Overall design: RNA from the e12.5 pituitaries of 3 WT and 2 KO littermate embryos was profiled.
Publication Title
Epithelial cell integrin β1 is required for developmental angiogenesis in the pituitary gland.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cells transiently adapt to hypoxia by globally decreasing protein translation. However, specific proteins needed to respond to hypoxia evade this translational repression. The mechanisms of this phenomenon remain unclear. We screened for and identified small molecules that selectively decrease HIF-2a translation in an mTOR independent manner, by enhancing the binding of Iron Regulatory Protein 1 (IRP1) to a recently reported Iron-Responsive Element (IRE) within the 5-untranslated region (UTR) of the HIF-2a message. Knocking down the expression of IRP1 by shRNA abolished the effect of the compounds. Hypoxia de-represses HIF-2a translation by disrupting the IRP1- HIF-2a IRE interaction. Thus, this chemical genetic analysis describes a molecular mechanism by which translation of the HIF-2a message is maintained during conditions of cellular hypoxia through inhibition of IRP-1 dependent repression. It also provides the chemical tools for studying this phenomenon.
Publication Title
Small-molecule inhibitors of HIF-2a translation link its 5'UTR iron-responsive element to oxygen sensing.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
In order to propagate a solid tumor, cancer cells must adapt to and survive under various tumor microenvironment (TME) stresses, such as hypoxia or lactic acidosis. To systematically identify genes that modulate cancer cell survival under stresses, we performed genome-wide shRNA screens under hypoxia or lactic acidosis. We discovered that genetic depletion of acetyl-CoA carboxylase (ACACA or ACC1) or ATP citrate lyase (ACLY) protected cancer cells from hypoxia-induced apoptosis. Additionally, loss of ACLY or ACC1 reduced levels and activities of the oncogenic transcription factor ETV4. Silencing ETV4 also protected cells from hypoxia-induced apoptosis and led to remarkably similar transcriptional responses as with silenced ACLY or ACC1, including an anti-apoptotic program. Metabolomic analysis found that while -ketoglutarate levels decrease under hypoxia in control cells, -ketoglutarate is paradoxically increased by hypoxia when ACC1 or ACLY are depleted. Supplementation with -ketoglutarate rescued the hypoxia-induced apoptosis and recapitulated the decreased expression and activity of ETV4 via an epigenetic mechanism. Therefore, ACC1 and ACLY regulate the levels of ETV4 under hypoxia via increased -ketoglutarate. These results reveal that ACC1/ACLY- -ketoglutarate-ETV4 is a novel means by which metabolic states regulate transcriptional output for life vs. death decisions under hypoxia. Since many lipogenic inhibitors are under investigation as cancer therapeutics, our findings suggest that the use of these inhibitors will need to be carefully considered with respect to oncogenic drivers, tumor hypoxia, progression and dormancy. More broadly, our screen provides a framework for studying additional tumor cell stress-adaption mechanisms in the future.
Publication Title
ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via α-ketoglutarate.
Sample Metadata Fields
Specimen part, Cell line
View Samples