Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of MYC-Low and MYC-High FC-MYC Cells Following SUMOylation Inhibition with SAEi ML-792

ABSTRACT: The synthetic lethal relationship between MYC and SAE2 has been previously described in FC-MYC cells using RNAi (Littler et al., 2019). Building on this work, we conducted transcriptomic analysis on MYC-low and MYC-high cells following inhibition of SUMOylation with the SAE1/2 inhibitor, ML-792 (SAEi). FC-MYC cells were grown for twenty-four hours in the absence (MYC-low) and presence (MYC-high) of 500ng/mL tetracycline and treated with either DMSO (vehicle control) or 25 nM SAEi for 24 hours. Three biological replicates were performed for RNAseq analysis, with additional subsets of cells reserved for complementary analyses, including DNA content profiling by flow cytometry and MYC protein expression analysis through western blotting. DNA content analysis showed that SAEi treatment had minimal affect on MYC-low cells but induced polyploidy and apoptosis in MYC-high cells. Western blotting confirmed MYC expression at the protein level as expected. This dataset provides transcriptomic profiles of MYC-low and MYC-high cells under SUMOylation inhibition, offering insights into the differential impact of SAEi on different MYC backgrounds. The dataset also includes analysis of parental RKO cells exposed to the SAEi.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER:

PROVIDER: E-MTAB-14654 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP166642

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Chromatin occupancy of key transcriptional regulators in P493-6 cells with various levels of c-Myc expression

Project description:P493-6 cells are immortalized human peripheral B cells that carry a conditional, tetracycline-regulated myc gene. We present ChIP-seq analysis of key transcritional regulators in P493-6 cells expressing various levels of c-Myc: 0hr (low c-Myc levels), 1hr (intermediate c-Myc levels), 24hr (very high c-Myc levels) and No Tet (steady-state c-Myc levels). Brd4, c-Myc, Max, Med1, RNAPII, and the chromatin modification H3K27Ac were profiled in P493-6 cells

2012-11-14 | E-GEOD-42262 | biostudies-arrayexpress

Gene expression analysis to identify Myc-regulated long noncoding RNAs in B cells with variable Myc levels

Project description:Myc is a well known transcription factor with important roles in cell cycle, apoptosis and cellular transformation. Long non-coding (lnc)RNAs have recently emerged as a important class of regulatory RNAs. Here, we show that lncRNAs are an extensive component of the Myc-regulated transcriptional program. Using the P493-6 inducible Myc model we demonstrate that both Myc-induced mRNAs and lncRNAs were significant enriched for Myc binding sites. In contrast to Myc-repressed mRNAs, Myc-repressed lncRNAs were significantly enriched for Myc binding sites. Subcellular localization analysis revealed that Myc-repressed lncRNAs and mRNAs are enriched in the nucleus while Myc-induced lncRNAs and mRNAs are enriched both in the cytoplasm and nucleus. Parallel analysis of differentially expressed lncRNAs and mRNAs identified 105 lncRNA-mRNA pairs that were in close vicinity, indicative for regulation in cis. To support the potential relevance of the Myc-regulated lncRNAs in cellular transformation, we analyzed their expression in primary Myc-high and Myc-low B-cell lymphomas. In total, 54% of the lncRNAs differentially expressed between the lymphoma subsets were identified as Myc-regulated in P493-6 cells. This study is the first to show that lncRNAs are an important factor within the Myc-regulated transcriptional program and indicates a marked difference between Myc-repressed lncRNAs and mRNAs. P493-6: 72h Tet treated (low c-myc levels), t=4h (intermediate c-myc levels), t=24h (high c-myc levels), untreated (steady state c-myc levels) Expression of all known mRNAs and >10 000 lncRNAs was assessed in P493-6 B cells with different c-myc levels

2015-02-01 | E-GEOD-59477 | biostudies-arrayexpress

Selective transcriptional regulation by Myc in cellular growth control and lymphomagenesis [ChIP-Seq]

Project description:The c-myc proto-oncogene product, Myc, is a transcription factor that binds thousands of genomic loci. Recent work suggested that rather than up- and down-regulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed "invasion") and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunoprecipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B-cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or mRNA copies per cell (hereby termed "amplification") when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, while having the potential to interact with all active/poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results imply that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover. Mapping c-Myc, RNAPII and H3K4me3, H3K4me1 and H3K27ac in four different models of Myc regulation Note: GEO Sample GSM894093 was used as input sample to generate processed data files P493.Myc.NoMyc.bed, P493.Myc.LowMyc.bed, P493.Myc.HighMyc.bed, P493.Myc.t1h.bed, P493.Myc.t24h.bed, P493.Pol2.NoMyc.bed, P493.Pol2.t24h.bed

2014-07-07 | E-GEOD-51004 | biostudies-arrayexpress

A sumoylation-dependent transcriptional subprogram is required for Myc-driven tumorigenesis

Project description:Myc is an oncogenic transcription factor frequently dysregulated in human cancer. To identify pathways supporting the Myc oncogenic program, we employed a genome-wide RNAi screen for Myc-synthetic-lethal (MySL) genes and uncovered a role for the SUMO-activating-enzyme (SAE1/2). Loss of SAE1/2 enzymatic activity drives synthetic lethality with Myc. Mechanistically, SAE2 inhibition switches a transcriptional subprogram of Myc from activated to repressed. A subset of these SUMOylation-dependent Myc-switchers (SMS genes) governs mitotic spindle function and is required to support the Myc oncogenic program. comparison of 4 treatments: normal HMEC, High Myc in HMEC, SUMO depleted in HMEC, High Myc+Sumo Depleted in HMEC

2011-12-08 | E-GEOD-34055 | biostudies-arrayexpress

Gene expression analysis in cytoplasmic and nuclear fractions of P493-6 B cells with low c-myc expression to assess long noncoding RNA localization

Project description:Myc is a well known transcription factor with important roles in cell cycle, apoptosis and cellular transformation. Long non-coding (lnc)RNAs have recently emerged as a important class of regulatory RNAs. Here, we show that lncRNAs are an extensive component of the Myc-regulated transcriptional program. Using the P493-6 inducible Myc model we demonstrate that both Myc-induced mRNAs and lncRNAs were significant enriched for Myc binding sites. In contrast to Myc-repressed mRNAs, Myc-repressed lncRNAs were significantly enriched for Myc binding sites. Subcellular localization analysis revealed that Myc-repressed lncRNAs and mRNAs are enriched in the nucleus while Myc-induced lncRNAs and mRNAs are enriched both in the cytoplasm and nucleus. Parallel analysis of differentially expressed lncRNAs and mRNAs identified 105 lncRNA-mRNA pairs that were in close vicinity, indicative for regulation in cis. To support the potential relevance of the Myc-regulated lncRNAs in cellular transformation, we analyzed their expression in primary Myc-high and Myc-low B-cell lymphomas. In total, 54% of the lncRNAs differentially expressed between the lymphoma subsets were identified as Myc-regulated in P493-6 cells. This study is the first to show that lncRNAs are an important factor within the Myc-regulated transcriptional program and indicates a marked difference between Myc-repressed lncRNAs and mRNAs. Arrays: The total, cy3 labeled fraction and the cytoplasmic or nuclear, cy5 labeled fraction was hybridized on the same array. Data was imported and analyzed as a single color array. Expression of all known mRNAs and >10 000 lncRNAs was assessed in P493-6 B cells with low c-myc levels

2015-02-01 | E-GEOD-59478 | biostudies-arrayexpress

Selective transcriptional regulation by Myc in cellular growth control and lymphomagenesis

Project description:The c-myc proto-oncogene product, Myc, is a transcription factor that binds thousands of genomic loci. Recent work suggested that rather than up- and down-regulating selected groups of genes, Myc targets all active promoters and enhancers in the genome (a phenomenon termed "invasion") and acts as a general amplifier of transcription. However, the available data did not readily discriminate between direct and indirect effects of Myc on RNA biogenesis. We addressed this issue with genome-wide chromatin immunoprecipitation and RNA expression profiles during B-cell lymphomagenesis in mice, in cultured B-cells and fibroblasts. Consistent with long-standing observations, we detected general increases in total RNA or mRNA copies per cell (hereby termed "amplification") when comparing actively proliferating cells with control quiescent cells: this was true whether cells were stimulated by mitogens (requiring endogenous Myc for a proliferative response) or by deregulated, oncogenic Myc activity. RNA amplification and promoter/enhancer invasion by Myc were separable phenomena that could occur without one another. Moreover, whether or not associated with RNA amplification, Myc drove the differential expression of distinct subsets of target genes. Hence, while having the potential to interact with all active/poised regulatory elements in the genome, Myc does not directly act as a global transcriptional amplifier. Instead, our results imply that Myc activates and represses transcription of discrete gene sets, leading to changes in cellular state that can in turn feed back on global RNA production and turnover. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-07-07 | E-GEOD-51011 | biostudies-arrayexpress

Revisiting Global Gene Expression Analysis (Microarray)

Project description:Gene expression analysis is a widely used and powerful method for investigating the transcriptional behavior of biological systems, for classifying cell states in disease and for many other purposes. Recent studies indicate that common assumptions currently embedded in experimental and analytical practices can lead to misinterpretation of global gene expression data. We discuss these assumptions and describe solutions that should minimize erroneous interpretation of gene expression data from multiple analysis platforms. RNA was extracted from cells expressing low or high levels of c-Myc. A panel of synthetic RNA's was added to these populations, based on cell number. Total RNA was then extracted and processed on Affymetrix microarrays in biological duplicate.

2012-10-25 | E-GEOD-40782 | biostudies-arrayexpress

MYC-ER and MYC-ER V394D induced gene expression changes in MCF10A cells

Project description:Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli and this protects long-lived organisms from cancer development. How cells discriminate physiological from supra-physiological levels of Myc is largely unknown. Here we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-sequencing experiments show that oncogenic levels of Myc, but not of MycV394D, a point mutant that does not bind Miz1, recruit Miz1 to core promoters and enable binding of Myc/Miz1 complexes to low-affinity target sites, correlating with repression of a specific set of target genes. Repressed genes encode proteins involved in cell adhesion, migration and wound healing; their promoters are enriched for binding sites of the serum response (SRF) factor. Restoring SRF activity attenuates Myc-induced apoptosis in response to glutamine starvation, exposure to Trail and to DNA damage. We propose that supra-physiological levels of Myc engage Miz1 in repressive DNA binding complexes and suppress transcriptional progr 4 different experimental conditions were analyzed: MYC-ER 4-OHT treated versus MYC-ER ctr-treated (EtOH), MYC-ER V394D 4-OHT treated versus MYC-ER V394D ctr-treated; 3 biological replicates for every condition.

2015-07-10 | E-GEOD-59145 | biostudies-arrayexpress

Analysis of MIZ1, MYC-ER and MYC-ERVD binding sites in MCF10A cells

Project description:Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli and this protects long-lived organisms from cancer development. How cells discriminate physiological from supra-physiological levels of Myc is largely unknown. Here we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-sequencing experiments show that oncogenic levels of Myc, but not of MycV394D, a point mutant that does not bind Miz1, recruit Miz1 to core promoters and enable binding of Myc/Miz1 complexes to low-affinity target sites, correlating with repression of a specific set of target genes. Repressed genes encode proteins involved in cell adhesion, migration and wound healing; their promoters are enriched for binding sites of the serum response (SRF) factor. Restoring SRF activity attenuates Myc-induced apoptosis in response to glutamine starvation, exposure to Trail and to DNA damage. We propose that supra-physiological levels of Myc engage Miz1 in repressive DNA binding complexes and suppress transcriptional progress. MIZ1, MYC-ER and MYC-ERVD ChIP-Seq with 10E2 and HC20 anti-ERalpha antibodies in MCF10A cells, performed on an Illumina IIx Genome Analyzer. Input sample is accessioned as GSM1423726.

2015-07-10 | E-GEOD-59146 | biostudies-arrayexpress

MYC-driven mouse HCC proteomics

Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").

2022-10-12 | PXD031478 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data