Murine MYC-dependent lymphoma cells: Dox vs. NoDox treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE12394 | GEO | 2008/08/12
SECONDARY ACCESSION(S): PRJNA113871
REPOSITORIES: GEO
Similar Datasets
Project description:miRNA expression profiling of murine MYC-dependent lymphoma cell lines harboring the MYC-transgene in a Tet-off system comparing control untreated lymphoma cells (high MYC expression state) with 18hours Dox treated lymphoma cells (low MYC expression state). Keywords: inducible expression system Two-condition experiment, Dox vs. NoDox treatment. Biological replicates: 26 distinct cell lines, 1 technical replicate. Four replicates per array.
2010-05-25 | E-GEOD-12394 | biostudies-arrayexpress
Project description:Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray.
2012-01-04 | GSE32129 | GEO
Project description:The MYC oncogene, which is commonly mutated/amplified in tumors, represents an important regulator of cell growth owing to its ability to induce both proliferation and apoptosis. Recent evidence links MYC to altered miRNA expression, thereby suggesting that MYC-regulated miRNAs might contribute to tumorigenesis. To further analyze the impact of MYC-regulated miRNAs we investigated a murine lymphoma model harboring the MYC transgene in a Tet-off system in order to control its expression. Microarray-based miRNA expression profiling revealed both known and novel MYC targets. Among the miRNAs repressed by MYC we identified the potential tumor suppressor miR-26a, which possessed the ability to attenuate proliferation in MYC-dependent cells. Interestingly, miR-26a was also found to be deregulated in primary human Burkitt lymphoma samples, thereby likely being of clinical relevance. While today only few miRNA targets have been identified in human disease, we could show that ectopic expression of miR-26a influenced cell cycle progression by targeting the bona fide oncogene EZH2, a Polycomb protein and global regulator of gene expression yet unknown to be regulated by miRNAs. Thus, in addition to directly targeting protein-coding genes, MYC modulates genes important to oncogenesis via deregulation of miRNAs, thereby vitally contributing to MYC-induced lymphomagenesis.
2008-07-31 | GSE12278 | GEO
Project description:The MYC oncogene, which is commonly mutated/amplified in tumors, represents an important regulator of cell growth owing to its ability to induce both proliferation and apoptosis. Recent evidence links MYC to altered miRNA expression, thereby suggesting that MYC-regulated miRNAs might contribute to tumorigenesis. To further analyze the impact of MYC-regulated miRNAs we investigated a murine lymphoma model harboring the MYC transgene in a Tet-off system in order to control its expression. Microarray-based miRNA expression profiling revealed both known and novel MYC targets. Among the miRNAs repressed by MYC we identified the potential tumor suppressor miR-26a, which possessed the ability to attenuate proliferation in MYC-dependent cells. Interestingly, miR-26a was also found to be deregulated in primary human Burkitt lymphoma samples, thereby likely being of clinical relevance. While today only few miRNA targets have been identified in human disease, we could show that ectopic expression of miR-26a influenced cell cycle progression by targeting the bona fide oncogene EZH2, a Polycomb protein and global regulator of gene expression yet unknown to be regulated by miRNAs. Thus, in addition to directly targeting protein-coding genes, MYC modulates genes important to oncogenesis via deregulation of miRNAs, thereby vitally contributing to MYC-induced lymphomagenesis. Experiment Overall Design: Gene expression profiling (GEP) was performed in six cell line samples using Affymetrix microarray technology according to the manufacturerâs recommendations (Human Genome U133 Plus 2.0 Array, Affymetrix). Fluorescence ratios were normalized by applying the RMA algorithm using the BRB Array Tools software package. For subsequent analyses, we only included probe sets whose expression varied as previously determined.
2008-10-31 | E-GEOD-12278 | biostudies-arrayexpress
Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. P493-6 cells which are Epstein-Barr virus-immortalized human B cells that harbor a tetracycline (tet)-repressible allele of Myc were studied. These cells are tumorigenic in immunocompromised mice and represent a model of human B cell lymphoma. miRNA expression profiles were examined in the high Myc (-tet) and low Myc (+tet) state. Keywords: Dose response P493 cells with high Myc (-tet) and low Myc (+tet) were compared.
2007-12-05 | E-GEOD-9070 | biostudies-arrayexpress
Project description:Regulation of gene expression programs is crucial for the survival of microbial pathogens in host environments and for their ability to cause disease. Here we investigated the epigenetic regulator RSC (Remodels the Structure of Chromatin) in the most prevalent human fungal pathogen Candida albicans. We addressed the global functions of RSC in C. albicans by analyzing the changes in the proteome of cells lacking the catalytic subunit Sth1 using DIA-MS (Data Independent Acquisition-Mass Spectrometry). For this purpose, we generated a conditional mutant harboring a doxycycline (dox)-repressible allele of STH1 (sth1∆/pTetO-STH1-MYC) and treated this mutant with dox for Sth1 depletion. To assess the effect of dox alone on gene expression, a near-isogenic sth1∆/STH1-MYC strain was also analysed.
2020-11-11 | PXD017990 | Pride
Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. P493-6 cells which are Epstein-Barr virus-immortalized human B cells that harbor a tetracycline (tet)-repressible allele of Myc were studied. These cells are tumorigenic in immunocompromised mice and represent a model of human B cell lymphoma. miRNA expression profiles were examined in the high Myc (-tet) and low Myc (+tet) state. Keywords: Dose response
2007-12-05 | GSE9070 | GEO
Project description:Mammary organoids harvested from ErbB3 DOX-KO mice, which utilize MMTV-Cre transgene expression in the LE to cause genomic recombination at floxed ErbB3 alleles in ErbB3FL/FL were cultured in the presence or absence of doxycycline to induce ErbB3 loss. The gene expression shift following DOX-induced ErbB3 loss in the 3D organoids was examined by microarray. Gene expression patterns were interrogated in mammary organoids from ErbB3 inducible-knockout mice cultured in the presence of absence of doxycycline. Three biological replicates of the experiment were performed, resulting in a total of 6 samples (3 treatment, 3 control).
2012-01-04 | E-GEOD-32129 | biostudies-arrayexpress
Project description:Strategies to overcome irreversible cochlear hair cell (HC) damage and loss are of vital importance to develop a treatment for hearing loss. HC regeneration in adult cochlea relies on a two-phase process: 1) Reprogramming mature cochlear (SCs) to regain the properties of their younger selves; 2) Activating Atoh1, a gene responsible for HC fate-determining, in the reprogrammed adult SCs for HC regeneration. We have shown that, by transient co-activation of Myc and NICD (Notch1 intracellular domain), the adult mouse cochlea can be successfully reprogrammed to a relatively younger stage and regain progenitor capacity, with the regeneration of HCs following Atoh1 overexpression in vitro and in vivo. To identify molecules to reprogram mature cochlear SCs, we utilized single-cell RNA sequencing and uncovered the pathways and their target genes underlying MYC/NICD-mediated reprogramming. We used an in-house adult cochlea explant culture system and carried out single-cell RNA sequencing to examine the gene expression profiles of cochlear explants from a transgenic mouse model, rtTa/tet-Myc/-tet-NICD, in response to Dox-induced MYC/NICD co-activation. We have shown that a 4-day treatment by Dox in cultured adult rtTa/tetMyc/-tet-NICD cochleae was sufficient to reprogram adult SCs for HC regeneration.
2022-06-03 | GSE205187 | GEO
Project description:Tet-on and tet-off systems are among the most popular vector systems for inducible transgene expression in mammalian cells. In tet-regulated systems the expression of the transgene depends on the presence or absence of the antibiotic tetracycline or its derivative doxycycline, which are added to the cell culture medium in concentrations considered to be far below cytotoxic levels. Therefore, potential effects on the treated cells, which are exerted by the antibiotic itself and unrelated to transgene expression, are often ignored. We examined the influence of low dose doxycycline on the transcriptional profile of two independent clones of MCF7 human breast carcinoma cells, transfected with tet-off regulator and response plasmids but not harboring any transgene. Treatment with 80 ng/ml doxycycline for 12 days markedly altered gene expression in these cells. Many genes associated with interferon-signaling were up-regulated while cell cycle-associated genes were down-regulated, which was also accompanied by a reduction of cell growth. These results highlight the importance of appropriate controls when working with tet-regulated gene expression systems, to allow distinction between the effects of transgene expression and potential “side effects” of the antibiotic used for its regulation.
2011-05-20 | GSE13926 | GEO