To study the effect of PIAS1 on transcriptional regulation, we establishedstable PIAS1 shRNA knockdown cells in breast cancer cell line MDA-MB231.
PIAS1 regulates breast tumorigenesis through selective epigenetic gene silencing.
Cell line, Treatment
View SamplesUHRF1 (Ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemimethylated DNA during replication, is essential for maintaining DNA methylation patterns during cell division and is suggested to direct additional repressive epigenetic marks. Uhrf1 mutation in zebrafish results in multiple embryonic defects including failed hepatic outgrowth, but the epigenetic basis of these phenotypes is not known. We find that DNA methylation is the only epigenetic mark that is depleted in uhrf1 mutants and make the surprising finding that despite the reduced organ size in uhrf1 mutants, genes regulating DNA replication and S-phase progression were highly upregulated. Further, there is a striking increase in BrdU incorporation in uhrf1 mutant cells, and they retained BrdU labeling over several days, indicating they are arrested in S-phase. Moreover, some of the label retaining nuclei co-localized with TUNEL positive nuclei, suggesting that arrested cells are responsible for apoptosis. Importantly, dnmt1 mutation phenocopies the S-phase arrest and hepatic outgrowth defects in uhrf1 mutants and Dnmt1 knock-down enhances the uhrf1 hepatic phenotype. Together, these data indicate that DNA hypomethylation is sufficient to generate the uhrf1 mutant phenotype by promoting an S-phase arrest. We thus propose that cell cycle arrest is a mechanism to restrict propagation of epigenetically deranged cells during embryogenesis.
DNA hypomethylation induces a DNA replication-associated cell cycle arrest to block hepatic outgrowth in uhrf1 mutant zebrafish embryos.
No sample metadata fields
View SamplesCompared the global gene expression profiles of HD- and CON-iPSC-derived neurons
Elucidating the role of the A2A adenosine receptor in neurodegeneration using neurons derived from Huntington's disease iPSCs.
Sex, Age, Specimen part
View SamplesThe goal of this study is to compare gene expression levels in uhrf1 mutants with global DNA hypomethylation to WT siblings Overall design: 10 whole embryos were pooled per sample of either 5 dpf old uhrf1 mutants or phenotypically WT siblings and RNA was extracted. Libraries were prepared according to Illumina Truseq RNA sample prep kit, version 2, followed by Ribo-Zero Gold treatment
Loss of DNA methylation in zebrafish embryos activates retrotransposons to trigger antiviral signaling.
No sample metadata fields
View SamplesUHRF1 is an essential regulator of DNA methylation that is highly expressed in many cancers. Using transgenic zebrafish, cultured cells and human tumors, we demonstrate that UHRF1 is an oncogene. RNAseq was used to assess the variation in gene expression between control and experimental samples. Overall design: Total small RNA from 2 batches of Tg(fabp10:has.UHRF1-GFP)High and age matched Tg(fabp10:nls-mCherry) control 5 dpf zebrafish livers was purified for preparation of high-throughput sequencing libraries.
UHRF1 overexpression drives DNA hypomethylation and hepatocellular carcinoma.
No sample metadata fields
View SamplesMacrophages in tumor microenvironment have been characterized as M1- and M2-polarized subtypes. This study sought to investigate the effects of different macrophage subtypes on the biological behavior and global gene expression profiles of lung cancer cells. Expression microarray and bioinformatics analyses indicated that the different macrophage subtypes mainly regulated genes involved in cell cycle, cytoskeletal remodeling, coagulation, cell adhesion and apoptosis pathways in A549 cells, a pattern that correlated with the altered behavior of A549 cells observed after coculture with macrophage subtypes.
Opposite Effects of M1 and M2 Macrophage Subtypes on Lung Cancer Progression.
Specimen part, Cell line
View SamplesIn order to identify patterns of gene expression associated with biological effects in THP-1 cells induced by F3, we performed a transcriptomic analysis on the THP-1 control and F3-treated THP-1 cells by oligonucleotide microarray
Ganoderma lucidum polysaccharides in human monocytic leukemia cells: from gene expression to network construction.
Cell line
View SamplesUsing RNA-seq to identify gene expression changes after genetic deletion of ADAR Overall design: RNA-seq of A549, HCC366, NCI-H1650, and NCI-H196 cells after CRISPR-Cas9-mediated deletion of ADAR as compared to a control gene. A549 cells were also treated with vehicle or interferon-ß for 24 hours prior to collection for RNA-seq.
Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells.
Cell line, Treatment, Subject
View SamplesThe CLS1/CAF co-culture maintained the cancer stemness. This cancer stemness was lost when the CAF feeder cells were removed during passaging.
Cancer-associated fibroblasts regulate the plasticity of lung cancer stemness via paracrine signalling.
Cell line
View SamplesThe study was designed in order to identify genes differentially expressed when glucocorticoid signaling is blocked by a glucocorticoid-receptor antagonist (RU486 mifepristone) in the context of brain inflammation induced by bacterial lipopolysaccharide (LPS). LPS is only able to cause murine brain damage in our experimental conditions upon RU486 pre-treatment. Hence, the study may reveal potential candidate genes to mediate neuroprotection or neurotoxicity. Due to the factorial design of the experiment, RU486 main-effect could be dissociated from the effects resultant of RU486/inflammation interaction. In addition, brain dissection was conducted to verify the effects in the brain side ipsilateral or contralateral to the site of intracerebral LPS infusion.
Genes involved in the balance between neuronal survival and death during inflammation.
Sex, Age, Specimen part
View Samples