Time-series analysis of response to ribosome 28s damage at gene expression level
Early Response to the Plant Toxin Stenodactylin in Acute Myeloid Leukemia Cells Involves Inflammatory and Apoptotic Signaling.
Cell line, Treatment
View SamplesThe goal of the study was to determine the effect of lentiviral- mediated overexpression of miR-495 (LV-miR-495) on the levels of gene expression in the nuclues accumbens of rats relative to control rats injected with the empty vector (LV-GFP).
In silico identification and in vivo validation of miR-495 as a novel regulator of motivation for cocaine that targets multiple addiction-related networks in the nucleus accumbens.
No sample metadata fields
View SamplesThe molecular events during nongenotoxic carcinogenesis and their temporal order are poorly understood but thought to include long-lasting perturbations of gene expression. Here, we have investigated the temporal sequence of molecular and pathological perturbations at early stages of phenobarbital (PB) mediated liver tumor promotion in vivo. Molecular profiling (mRNA, microRNA [miRNA], DNA methylation, and proteins) of mouse liver during 13 weeks of PB treatment revealed progressive increases in hepatic expression of long noncoding RNAs and miRNAs originating from the Dlk1-Dio3 imprinted gene cluster, a locus that has recently been associated with stem cell pluripotency in mice and various neoplasms in humans. PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, sug- gesting a role for -catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs. The carcinogenic relevance of Dlk1-Dio3 locus ncRNA induction was further supported by in vivo genetic dependence on constitutive androstane receptor and -catenin pathways. Our data identify Dlk1-Dio3 ncRNAs as novel candidate early biomarkers for mouse liver tumor promotion and provide new opportunities for assessing the carcinogenic potential of novel compounds.
Identification of Dlk1-Dio3 imprinted gene cluster noncoding RNAs as novel candidate biomarkers for liver tumor promotion.
Specimen part
View SamplesChronic loss of Lasp1 alters the expression of other genes associated with cell motility/attachment, and/or other cellular functions. Results provide new information showing that loss of Lasp1 leads to up- and down-regulation of genes involved in cell motility/attachment/growth.
Lasp1 gene disruption is linked to enhanced cell migration and tumor formation.
No sample metadata fields
View SamplesHNF4a is an important liver transcription factor that regulates at least a thousand genes in the liver. Here we used expression profiling in HepG2 cells, a hepatocellular carcinoma cell line, in which HNF4a was knocked down by RNAi to identify some of those target genes. This dataset accompanies the article in Hepatology 2010 Feb;51(2):642-53. Integrated approach for the identification of human hepatocyte nuclear factor 4alpha target genes using protein binding microarrays by Bolotin E, Liao H, Ta TC, Yang C, Hwang-Verslues W, Evans JR, Jiang T, Sladek FM.
Integrated approach for the identification of human hepatocyte nuclear factor 4alpha target genes using protein binding microarrays.
Cell line
View SamplesCells undergoing malignant transformation often shift their cellular metabolism from primarily oxidative phosphorylation to aerobic glycolysis (the Warburg effect). Energy restriction-mimetic agents (ERMAs), such as 2-deoxyglucose and resveratrol, that target this shift in cellular metabolism have been effective in inhibiting cancer cell growth in vitro, and xenograft tumor growth in vivo.
Suppression of prostate epithelial proliferation and intraprostatic progrowth signaling in transgenic mice by a new energy restriction-mimetic agent.
Specimen part
View SamplesProphase I of male meiosis involves dynamic chromosome segregation processes during early spermatogenesis, including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility in humans, we performed expression profiling of mouse spermatogenic cells undergoing meiotic prophase I.
Screening of genes involved in chromosome segregation during meiosis I: toward the identification of genes responsible for infertility in humans.
Sex, Specimen part
View SamplesProphase I of meiosis involves dynamic chromosome segregation processes including synapsis, meiotic recombination, and cohesion. Genetic defects in genes participating in these processes consistently cause reproduction failure in mice. To identify candidate genes responsible for infertility or recurrent pregnancy loss in humans, we performed expression profiling of male and female gonads of mice undergoing meiotic prophase I.
Screening of genes involved in chromosome segregation during meiosis I: in vitro gene transfer to mouse fetal oocytes.
Sex, Age, Specimen part
View SamplesNOD mice were injected once a week with LTBR-Ig to block the LTBR-pathway, or with control monoclonal antibody MOPC from age 8 to 16 weeks old. Extraorbital lacrimal glands or submaxillary glands were dissected and total mRNA prepared. Each sample was either the combined lacrimals (2) from each mouse or individual salivary glands. There were 4 mice in each treatment group. Total mRNA was isolated and the quality was assessed using the Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Reverse transcription to prepare cDNA was performed using Invitrogen M-MLV system. The purpose was to determine changes in gene expression in glands due to blockade of the LTBR-pathway.
Lymphotoxin-beta receptor blockade reduces CXCL13 in lacrimal glands and improves corneal integrity in the NOD model of Sjögren's syndrome.
Specimen part, Treatment, Time
View SamplesPurpose: Aim of the study is to identify functional differences between the P1 and P2-HNF4a isoforms. To do this, we generated Tet-On inducible lines that express either the human (P1) HNF4a2 or (P2) HNF4a8 under control of DOX in the HCT116 human colon cancer cells. Methods: HNF4a2 and Parental lines were induced with 0.3 µg/mL DOX, while HNF4a8 line was induced with either 0.1 or 0.3 µg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the Illumina TruSeq RNA. Result: There were common and unique dysregulated genes identified in the HNF4a2 and HNF4a8 lines (+DOX); more upregulated genes than downregulated genes in both the lines. Conclusion: The functional difference between HNF4a2 and HNF4a8 is that the latter tends to upregulate genes involved in proliferation and anti-apoptosis while HNF4a2 upregulates genes involved in growth suppression and cell death. Overall design: Tet-On inducible HCT116 cell (Parental, HNF4a2, and HNF4a8) lines, treated with (0.0, 0.1, or 0.3 µg/mL) DOX for 24 hours, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.
Differential Effects of Hepatocyte Nuclear Factor 4α Isoforms on Tumor Growth and T-Cell Factor 4/AP-1 Interactions in Human Colorectal Cancer Cells.
No sample metadata fields
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