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Use the form below to search 9,145 publicly available datasets published in the Gene Expression Omnibus database and processed by ARCHS4.

 
Expression data for HT29 cells treated with 5-aza-deoxy-cytidine [RNA-Seq]
GSE41586
9 samples
Published September 2013
Summary
The RNA samples from HT-29 (ATCC) colon cancer cell line were reverse transcribed to build cDNA libraries and categorized into 3 groups with different concentrations of 5-aza-deoxy-cytidine (5-Aza); in each group three replicative 150 mm cultures were treated with: 1) dimethyl sulfoxide (vehicle alone, 0 μM 5-Aza); 2) 5μM 5-Aza and 3) 10 μM 5-Aza; for five days. This experiment was also performed parallel on a commercial Affymetrix microarray [GSE41364] and the aim of the study was to compare the two platforms on gene expression measurements and differentially expressed gene (DEG) detection. The results showed a strong correlation between the two platforms, yet it also confirmed the existence of fixed and proportional biases on the gene expression measurements between microarray and RNA-Seq. The DEG analysis indicated the relative superiority of DESeq method in terms of its performance; high consistency was confirmed between DESeq, baySeq methods from RNA-Seq and SAM/eBayes from microarray data.
Organism
Homo sapiens
Regulation of constitutive and alternative splicing by PRMT5 reveals a role for Mdm4 pre-mRNA in sensing defects in the spliceosomal machinery (RNA-Seq)
GSE45284
12 samples
Published September 2013
Summary
Protein Arginine MethylTransferase 5 (PRMT5) is known to mediate epigenetic control on chromatin and to functionally regulate components of the splicing machinery. In this study we show that selective deletion of PRMT5 in different organs leads to cell cycle arrest and apoptosis. At the molecular level, PRMT5 depletion results in reduced methylation of Sm proteins, aberrant constitutive splicing and in the Alternative Splicing (AS) of specific mRNAs. We identify Mdm4 as one of these mRNAs, which due to its weak 5’-Donor site, acts as a sensor of splicing defects and transduces the signal to activate the p53 response, providing a mechanistic explanation of the phenotype observed in PRMT5 conditional knockout mice. Our data demonstrate a key role of PRMT5, together with p53, as guardians of the transcriptome. This will have fundamental implications in our understanding of PRMT5 activity, both in physiological conditions, as well as pathological conditions, including cancer and neurological diseases.
Organism
Mus musculus
LncRNA-dependent mechanisms of androgen receptor-regulated gene activation programs [GRO-seq II]
GSE47806
6 samples
Published August 2013
Summary
While thousands of long non-coding RNAs (lncRNAs) are expressed in higher eukaryotes, the potential regulatory roles of lncRNAs in regulated gene transcription programs remain rather poorly understood. Here, we report that two lncRNAs highly overexpressed in aggressive prostate cancer, PRNCR1 and PCGEM1, bind successively to the androgen receptor (AR) and strongly enhance both ligand-dependent and ligand-independent AR-mediated gene activation programs and proliferation in prostate cancer cells. Binding of PRNCR1 to the C-terminally acetylated AR on enhancers and its association with DOT1L appear to be required for recruitment of the second lncRNA, PCGEM, to the N-terminally methylated AR. Unexpectedly, recognition of the H3K4me3 promoter mark by the PHD finger-domain of Pygopus2, recruited by PCGEM1, proves to enhance selective looping of AR-bound enhancers to target gene promoters in these cells, revealing a novel aspect of ligand-induced enhancer-promoter interactions. In “resistant” prostate cancer cells, these overexpressed lncRNAs can interact with, and are required for the robust activation of both truncated and full length AR, causing DHT-independent activation of the AR transcriptional program and cell proliferation. Conditionally-expressed short hairpin RNA (shRNA)-mediated targeting of these lncRNAs in these resistant cancer cell lines strongly suppressed xenograft growth in vivo. Together, these results suggest that these overexpressed lncRNAs can potentially serve as a required component of castration-resistance in prostatic tumors.
Organism
Homo sapiens
Long-term exposure to low-concentrations of Cr(VI) induce DNA damage and disrupt the transcriptional response to benzo[a]pyrene
GSE49571
20 samples
Published August 2013
Summary
Living organisms are exposed on a daily basis to widespread mixtures of toxic compounds. Mixtures pose a major problem in the assessment of health effects because they often generate substance-specific effects that cannot be attributed to a single mechanism. Two compounds often found together in the environment are the heavy metal chromium and the polycyclic aromatic hydrocarbon benzo[a]pyrene (B[a]P). We have examined how long-term exposure to a low concentration of Cr(VI) affects the transcriptional response to B[a]P, a second toxicant with an unrelated mechanism of action. Growth of mouse hepatoma cells for 20 passages in medium with 0.1 or 0.5 uM Cr(VI) increases DNA damage and apoptosis and decreases clonogenic ability. These cells also show transcriptome changes indicative of increased expression of DNA damage response and repair genes. In them, B[a]P activates cancer progression pathways, unlike cells never exposed to Cr(VI), where B[a]P activates mostly xenobiotic metabolism pathways. Cells grown in Cr(VI) for 20 passages and then cultured for an additional 5 passages in the absence of Cr(VI) recover from some but not all the chromium effects. They show B[a]P-dependent transcriptome changes strongly weighted towards xenobiotic metabolism, similar to those in B[a]P-treated cells that had no previous Cr(VI) exposure, but retain a high level of Cr(VI)-induced DNA damage and silence the expression of DNA damage and cancer progression genes. We conclude that the combined effect of these two toxicants appears to be neither synergistic nor cumulative, generating a toxic/adaptive condition that cannot be predicted from the effect of each toxicant alone.
Organism
Mus musculus
De novo sequencing of circulating microRNAs in locally advanced breast cancer
GSE49035
42 samples
Published July 2013
Summary
MicroRNAs (miRNAs) have been recently detected in the circulation of cancer patients, where they are associated with clinical parameters. Discovery profiling of circulating small RNAs has not been previously reported in breast cancer (BC), and was carried out in this study to identify blood-based small RNA markers of BC clinical outcome.
Organism
Homo sapiens
Lineage analysis of basal epithelial cells reveals their unexpected plasticity and supports a cell of origin model for prostate cancer heterogeneity
GSE39509
34 samples
Published January 2013
Summary
We used RNA-seq to compare the expression profiles of mouse prostate tumors originated from epithelial basal cells to those originated from luminal cells. We next generated expression signatures for both basal and luminal origin tumors by comparison of tumor samples to their respective controls. By comparing luminal to basal signatures we identified a prognostic molecular signature for prostate cancer patient survival.
Organism
Mus musculus
Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of binding sites in a cell type-specific manner
GSE38234
16 samples
Published June 2012
Summary
To obtain an integrated view of gene regulation in response to environmental and endogenous estrogens on a genome-wide scale, we performed ChIP-seq, to identify estrogen receptor 1 (ER) binding sites, and RNA-seq in endometrial cancer cells exposed to bisphenol A (BPA; found in plastics), genistein (GEN; found in soybean), or 17β-estradiol (E2; an endogenous estrogen).  GEN and BPA treatment induces thousands of ER binding sites and >50 gene expression changes, representing a subset of E2‑induced gene regulation changes. Genes affected by E2 were highly enriched for ribosome-associated proteins; however, GEN and BPA failed to regulate most ribosome-associated proteins and instead enriched for transporters of carboxylic acids. Treatment-dependent changes in gene expression were associated with treatment-dependent ER binding sites, with the exception that many genes up-regulated by E2 harbored a BPA-induced ER binding site, but failed to show any expression change after BPA treatment. GEN and BPA exhibited a similar relationship to E2 in the breast cancer line T-47D, where cell type specificity played a much larger role than treatment specificity. Overall, both environmental estrogens clearly regulate gene expression through ER on a genome-wide scale, although with lower potency resulting in less ER binding sites and less gene expression changes compared to the endogenous estrogen, E2.
Organism
Homo sapiens
Effects of Cardiac Glycosides on RNA Expression in Prostate Cancer LNCaP-abl Cells
GSE35126
6 samples
Published April 2012
Summary
Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown.
Organism
Homo sapiens
Gene expression of polyoma middle T antigen induced mammary tumors [RNA_Seq : MOLF x PyMT]
GSE31223
14 samples
Published August 2011
Summary
Mouse genetic crosses were established between the PyMT model of metastatic breast cancer and MOLF strain. Tumors were harvested from the animals for gene expression analysis to identify genes and network modules associated with progression to distant metastatic disease.
Organism
Mus musculus