Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic and Epigenetic analysis of cell line derivatives from H2087 and HCC1954 cell lines

ABSTRACT: We profiled the transcriptomes of latency-competent cells derived from the human cancer cell lines H2087 (lung adenocarcinoma) and HCC1954 (breast adenocarcinoma) in mitogen-rich and mitogen-low media (MRM and MLM, respectively). In addition, we analyzed the epigenetic landscape of these cell lines under MLM conditions. H2087 and HCC1954 parental and latency-competent cell derivatives (LCCs) were grown for 48hr in mitogen-rich or mitogen-low conditions in vitro, and whole RNA was extracted for RNA-seq profiling. Cell lines were also grown in MLM conditions and DNA extracted for ChIP-Seq experiments.

ORGANISM(S): Homo sapiens

SUBMITTER: Danilo Macalinao

PROVIDER: E-GEOD-72956 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Metastatic Latency and Immune Evasion through Autocrine Inhibition of WNT.

Malladi Srinivas S Macalinao Danilo G DG Jin Xin X He Lan L Basnet Harihar H Zou Yilong Y de Stanchina Elisa E Massagué Joan J

Cell 20160301 1

Metastasis frequently develops years after the removal of a primary tumor, from a minority of disseminated cancer cells that survived as latent entities through unknown mechanisms. We isolated latency competent cancer (LCC) cells from early stage human lung and breast carcinoma cell lines and defined the mechanisms that suppress outgrowth, support long-term survival, and maintain tumor-initiating potential in these cells during the latent metastasis stage. LCC cells show stem-cell-like character ...[more]

PMID: 27015306

Similar Datasets

TGF-Î² Tumor Suppression Through A Lethal EMT

Project description:TGF-Î² is a major tumor suppressor in gastrointestinal (GI) and squamous carcinomas, which exhibit frequent genetic inactivation of Smad4, a key TGF-Î² signaling component. Apoptosis is implicated as an important mediator of the tumor suppressive function of TGF-Î², although this process remains poorly understood. To address this long-standing question, we dissected the tumor suppressive action of TGF-Î² in naÃ¯ve pancreatic ductal adenocarcinoma (PDA) cells. Here we show that TGF-Î²/Smad4 signaling triggers an EMT in Kras-mutant pancreatic progenitor cells but turns this process into a trigger of apoptosis by converting the progenitor cell transcription factor Sox4 from an enforcer of epithelial progenitor identity into an activator of apoptosis. This occurs as a result of the EMT-linked repression of the endodermal master regulator Klf5, which cooperates with Sox4 to promote epithelial progenitor identity, and loss of which unmasks a latent apoptotic transcriptional program driven by Sox4. By losing Smad4, Kras-mutant PDA cells avoid this fate and instead use Sox4 as a TGF-Î²-dependent enforcer of the epithelial progenitor cell state. In this study, 16 RNA-Seq samples and 6 ChIP-Seq samples are included.

2016-02-24 | E-GEOD-72069 | biostudies-arrayexpress

FAIRE-seq 1,25(OH)2D3 time course in THP-1 cells

Project description:Assessment of regions of open chromatin by FAIRE-seq in THP-1 cells treated with 1,25(OH)2D3 for 0-48 h Three independent experiments of 1,25(OH)2D3 time course in THP-1 cells

2016-07-04 | E-GEOD-69297 | biostudies-arrayexpress

CTCF ChIP-seq in human monocytic THP-1 cells

Project description:ChIP-seq for the insulator protein CTCF in THP-1 cells after stimulation with the the natural VDR ligand 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) THP-1 cells were treated for 24 h with 100 nM 1,25(OH)2D3 before ChIP assay

2016-07-04 | E-GEOD-69962 | biostudies-arrayexpress

Genome-wide map of JMJD1C binding in Kasumi-1 cells [ChIP-seq]

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of JMJD1C and LYL1 chromatin binding in Kasumi-1 cells, HL-60 cells, NB-4 cells and THP-1 cells, including ChIP-seqs of JMJD1C and LYL1, and input DNAs for Kasumi-1, HL-60, NB4.

2015-11-02 | E-GEOD-63484 | biostudies-arrayexpress

RNA-seq 1,25(OH)2D3 time course in THP-1 cells

Project description:gene expression profiling by RNA-seq in THP-1 cells treated with 1,25(OH)2D3 for 2.5-24 h three independent experiments of 1,25(OH)2D3 time course in THP-1 cells

2016-07-04 | E-GEOD-69284 | biostudies-arrayexpress

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of RNA expression when Kasumi-1 cells are treated with control shRNA or two different JMJD1C shRNAs; in duplicate. Please note that the 'shAML1_ETO_vs_shControl.all_gene_exp.tb.txtl' was generated comparing control and shRNA treated RNA abundance-using previously published data [GSE43834; GSM1071857 and GSM1071852].

2015-11-02 | E-GEOD-63485 | biostudies-arrayexpress

The BCL6 RD2 domain governs commitment of activated B-cells to form germinal centers

Project description:Our data demonstrated that Bcl6 directly binds and represses trafficking receptors S1pr1 and Grp183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B-cell migration and may contribute to the Germinal Center failure in Bcl6RD2MUT mice. RNAseq was performed in endogenous BCL6-depleted OCI-LY1 cells rescued with either WT or RD mutant BCL6 (N=3 for each group).

2014-09-14 | E-GEOD-58365 | biostudies-arrayexpress

Bromodomain inhibition of the transcriptional coactivators CBP/EP300 as a therapeutic strategy to target the IRF4 network in multiple myeloma (ChIP-Seq)

Project description:Pharmacological inhibition of chromatin co-regulatory factors represents a clinically validated strategy to modulate oncogenic signaling through selective attenuation of gene expression. Here, we demonstrate that CBP/EP300 bromodomain inhibition preferentially abrogates the viability of multiple myeloma cell lines. Phenotypic effects are preceded by the direct transcriptional suppression of the lymphocyte-specific transcription factor IRF4 and the subsequent down-regulation of the IRF4 transcriptional program. Ectopic expression of IRF4 antagonizes the phenotypic effects of CBP/EP300 bromodomain inhibition and prevents the suppression of the IRF4 target c-MYC. These findings suggest that CBP/EP300 bromodomain inhibition represents a viable therapeutic strategy for targeting multiple myeloma and other lymphoid malignancies dependent on the IRF4 network. A total of 13 ChIP-seq samples were sequenced. Samples were treated with control (DMSO) or test compound (2.5 uM SGC-CBP30 or 0.25uM CPI267203) for 6 hours. Signal from input samples was included to subtract background signal from each ChIP-seq sample. Antibodies used were against p300, H3K18ac, H3K27ac, or BRD4.

2016-01-05 | E-GEOD-71909 | biostudies-arrayexpress

Inhibitors of the histone lysine demethylase KDM1A are broadly efficacious in AML by evicting the enzyme from chromatin [ChIP-Seq]

Project description:Examine the distribution of KDM1A and the histone H3K4me2 mark on chromatin following treatment with two distinct classes of KDM1A inhibitors - an irreversible inhibitor (RN-1) and a reversible inhibitor (GSK690) 15 samples total from two treated cell lines - 9 from Kasumi-1 and 6 from SKNO-1. Controls included were input DNA isolated from the treated cells.

2016-02-10 | E-GEOD-71739 | biostudies-arrayexpress

Timecourse total transcriptome sequencing of MCF10A cells undergoing acinus formation.

Project description:RNA-seq was performed for transcriptional analysis of MCF10A cells, an epithelial mammary cell line. MCF10A cells were cultured in 3D acinus forming conditions (in Matrigel). Timepoints analysed were 24h, 34h, 36h, 38h and 48h into acinus formation. Control cells were monoloayer.

2014-10-02 | E-MTAB-2969 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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