Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide modelling of transcription kinetics reveals patterns of RNA processing delays

ABSTRACT: We descrive a joint model of transcriptional activation and mRNA accumulation, using estrogen receptor ERα activation in MCF-7 breast cancer cell line, which can be used for inference of transcription rate, RNA processing delay and degradation rate given data from high-throughput sequencing time course experiments.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62789 | GEO | 2015/03/04

SECONDARY ACCESSION(S): PRJNA265118

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide modelling of transcription kinetics reveals patterns of RNA processing delays

Project description:We descrive a joint model of transcriptional activation and mRNA accumulation, using estrogen receptor ERM-NM-1 activation in MCF-7 breast cancer cell line, which can be used for inference of transcription rate, RNA processing delay and degradation rate given data from high-throughput sequencing time course experiments. MCF-7 cells were mock treated or with 10nM 17b-E2 to nine time points (5', 10', 20', 40', 80', 160', 320', 640' and 1280'). Genome-wide identification of RNA polymerase II (RNAPII) occupancy and transcriptome profiling (RNA-seq) following E2 induction of MCF-7 cells Please note that the information in the wig.txt files is in gene-specific coordinates, not chromosomic coordinates, as this is the most sensible format for the associated project/paper.

2015-03-04 | E-GEOD-62789 | biostudies-arrayexpress

Genome-wide modelling of transcription kinetics reveals patterns of RNA processing delays

Project description:We descrive a joint model of transcriptional activation and mRNA accumulation, using estrogen receptor ERα activation in MCF-7 breast cancer cell line, which can be used for inference of transcription rate, RNA processing delay and degradation rate given data from high-throughput sequencing time course experiments. MCF-7 cells were mock treated or with 10nM 17b-E2 to nine time points (5', 10', 20', 40', 80', 160', 320', 640' and 1280'). Genome-wide identification of RNA polymerase II (RNAPII) occupancy and transcriptome profiling (RNA-seq) following E2 induction of MCF-7 cells Please note that the information in the wig.txt files is in gene-specific coordinates, not chromosomic coordinates, as this is the most sensible format for the associated project/paper.

| S-ECPF-GEOD-62789 | biostudies-other

P21-activated kinase group II small compound inhibitor GNE-2861 perturbs estrogen receptor alpha signaling and restores tamoxifen-sensitivity in breast cancer cells

Project description:Estrogen receptor alpha (ERα) is highly expressed in most breast cancers. Consequently, ERα modulators, such as tamoxifen, are successful in breast cancer treatment, although tamoxifen resistance is commonly observed. While tamoxifen resistance may be caused by altered ERα signaling, the molecular mechanisms regulating ERα signaling and tamoxifen resistance are not entirely clear. Here, we found that PAK4 expression was consistently correlated to poor patient outcome in endocrine treated and tamoxifen-only treated breast cancer patients. Importantly, while PAK4 overexpression promoted tamoxifen resistance in MCF-7 human breast cancer cells, pharmacological treatment with a group II PAK (PAK4, 5, 6) inhibitor, GNE-2861, sensitized tamoxifen resistant MCF-7/LCC2 breast cancer cells to tamoxifen. Mechanistically, we identified a regulatory positive feedback loop, where ERα bound to the PAK4 gene, thereby promoting PAK4 expression, while PAK4 in turn stabilized the ERα protein, activated ERα transcriptional activity and ERα target gene expression. Further, PAK4 phosphorylated ERα-Ser305, a phosphorylation event needed for the PAK4 activation of ERα-dependent transcription. In conclusion, PAK4 may be a suitable target for perturbing ERα signaling and tamoxifen resistance in breast cancer patients.

2015-12-12 | GSE73320 | GEO

Genomic encoding of transcriptional burst kinetics

Project description:We used single-cell RNA-sequencing to generate allele-resolution expression levels in individual cells that we used for inference of transcriptional burst kinetics.

2018-09-30 | E-MTAB-6362 | biostudies-arrayexpress

Differential chromatine state and ER binding potentially induced by NR2F2 depletion.

Project description:ERα binding activity largely depends on access to binding sites on chromatin, which is facilitated in part by Pioneer Factors (PFs).We show that most binding events of NR2F2 occur together with the ERα binding sites.To explore whether NR2F2 may act as potential pioneer factor of ER, we performed a series of ChIP-seq genome wide in MCF-7. Since NR2F2 associates with chromatin prior to estrogen treatment and its depletion in MCF-7 cells did not affect ERα expression, we hypothesize NR2F2 may inhibit estrogen-dependent growth by modulating ERα recruitment. We performed ChIP-seq genome wide gainst ERα before and after NR2F2 depletion.Covalent modifications are a main chromatin property.To test whether NR2F2 favoured histone modification deposition on chromatin, we profiled ChIP-Seq of H3K4me1, H3K4me3, and H3K27ac following NR2F2 depletion in oestrogen-starved MCF-7 cells to gain comprehensive histone medication landscape.

2019-10-15 | GSE132432 | GEO

AKT Isoform Specificity Downstream of PIK3CA Mutation Impacts Estradiol and PI3K Inhibitor Response in Breast Cancer Cells

Project description:Background: PIK3CA mutations are observed in >30% of breast cancers, which are more common in estrogen receptor (ERα)-positive breast cancer compared with ERα-negative breast cancer. AKT1, 2, and 3 isoforms, major isoforms downstream of PI3K, modulate ERα activity. It is unknown whether PIK3CA mutation leads to preferential activation of specific AKT isoforms with an ability to modulate ERα function. Methods: Gene expression arrays were performed on parental, AKT1 knockdown or AKT2 knockdown MCF-7 breast cancer cells with or without estradiol treatment for three hours. Results: AKT1 had a dominant role in ERα:estradiol-dependent gene expression and proliferation. We have identified a unique gene expression signature that is dependent on ERα, estradiol, AKT1 and the pioneer factor FOXA1. Overexpression of this signature was associated with better outcome in patients with ERα-positive breast cancer. In contrast, AKT2 controlled global gene expression.

2016-08-10 | GSE60759 | GEO

Interleukin-6 is a Potential Therapeutic Target in Interleukin-6 Dependent Estrogen Receptor-alpha Positive Breast Cancer [cell lines]

Project description:Interleukin-6 (IL-6) is an important growth factor for estrogen receptor-alpha (ERα) positive breast cancer, and elevated serum IL-6 is associated with poor prognosis. We firstly demonstrated that pSTAT3 is the primary downstream IL-6 signaling pathway in ERα-positive breast cancer, using ten different breast cancer cell lines. Three-dimensional cultures of these cell lines were also used to develop a 17-gene IL-6 specific gene signature that could be used to identify IL-6 driven disease. This signature included a variety of genes involved in immune cell function and migration, cell growth and apoptosis, and the tumor microenvironment. To further validate this IL-6 signature, we obtained 36 human ERα-positive breast cancer tumor samples with matched serum for gene expression profiling and determination of an IL-6 pathway activation score (PAS). Patients with high IL-6 PAS were also enriched for elevated serum IL-6 (>=10 pg/ml). We then utilized a murine MCF-7 xenograft model to determine the role of IL-6 in ERα-positive breast cancer and potential anti-IL-6 therapy in vivo. When IL-6 was administered in vivo, MCF-7 cells engrafted without the need for estrogen supplementation. Subsequently, we prophylactically treated mice at MCF-7 engraftment with an anti-IL-6 antibody (siltuximab), fulvestrant or combination therapy. Siltuximab alone was able to blunt MCF-7 engraftment. Similarly, when tumors were allowed to grow to 125 mm3 before treatment, siltuximab alone demonstrated tumor regressions in 90% (9/10) of tumors. Given the established role for IL-6 in ERα+ breast cancer, this data demonstrates the potential for anti-IL-6 therapeutics.

2016-02-04 | GSE54329 | GEO

Interleukin-6 is a Potential Therapeutic Target in Interleukin-6 Dependent Estrogen Receptor-alpha Positive Breast Cancer [patient tumor tissue]

2016-02-04 | GSE54330 | GEO

RNA-seq on MCF7 cells induced with sgRNA vectors targeting CTCF binding elements

Project description:We performed a CRISPR-based functional genetic screen targeting CTCF binding elements (CBEs) located in the vicinity of ERα-bound enhancers. The screen identified four functional CBEs whose targeting resulted in a marked negative effect on the proliferation of MCF-7 cells (ERα-positive cells) but no significant effect on MDA-MB-231 (ERα-negative cells) cells. We then carried out RNA-seq analysis on MCF-7 cells induced with sgRNA vectors targeting these four CBEs: sgRNA_1118, sgRNA_1659, sgRNA_680 and sgRNA_810, as well as non-targeting sgRNA as control.

2019-11-01 | GSE124573 | GEO

GRO-seq on MCF7 cells induced with sgRNA vectors targeting CTCF binding elements

Project description:We performed a CRISPR-based functional genetic screen targeting CTCF binding elements (CBEs) located in the vicinity of ERα-bound enhancers. The screen identified four functional CBEs whose targeting resulted in a marked negative effect on the proliferation of MCF-7 cells (ERα-positive cells) but no significant effect on MDA-MB-231 (ERα-negative cells) cells. Here, we carried out GRO-seq analysis on MCF-7 cells induced with an sgRNA vector targeting one of the hits detected by the screen: sgRNA_1118, as well as non-targeting sgRNA and sg1830 as control.

2019-11-01 | GSE124572 | GEO

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