Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Hypoxia-related Transcription factor ChIP-Seq data in T47D breast cancer cells

PROVIDER: PRJNA257093 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR1532952.fastq.gz	Fastqsanger.gz
	SRR1532953.fastq.gz	Fastqsanger.gz
	SRR1532954.fastq.gz	Fastqsanger.gz
	SRR1532955.fastq.gz	Fastqsanger.gz
	SRR1532956.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Project description:Hypoxia-related transcription factor ChIP-seq and EglN2 knockdown expression profiling in T47D breast cancer cells

| PRJNA257092 | ENA

T47D Breast cancer cell line ChIP-seq data

Project description:T47D Breast cancer cell line ChIP-seq data

| PRJNA415426 | ENA

Expression data with either EglN2 or control knockdown in T47D cells

Project description:In order to perform integrated analysis for EglN2 ChIP-Seq and microarray to identify EglN2 direct target genes, we performed the microarray analysis for T47D breast cancer cells with either control or EglN2 siRNA followed by hypoxia+DMOG treatment T47D cells were transfected with either control or EglN2 siRNA in duplicate with RNAi max. 36 hours following transfection, cells were treated with hypoxia (1%) and DMOG (1 mM) for 16 hours. Following treatment, total RNA was extracted using Rnaeasy kit from Qiagen.

2014-07-31 | E-GEOD-59936 | biostudies-arrayexpress

Project description:We report the comprehensive genome-wide binding peaks for key factors inovled in oxygen sensing pathways, such as HIF1α, HIF1β and EglN2. In addition, we also report the genome-wide binding peaks for NRF1 in breast cancer cells We conducted HA-EglN2, HIF1α, HIF1β (ARNT) or NRF1 ChIP-Seq in the T47D cell line that overexpresses HA-EglN2 in the presence of hypoxia (1%) and DMOG treatment. T47D parental cells treated with the same condition followed by HA ChIP-seq served as the control to filter non-specific binding.

2014-07-31 | E-GEOD-59935 | biostudies-arrayexpress

Expression data with either EglN2 or control knockdown in T47D cells

2014-07-31 | GSE59936 | GEO

T47D Breast cancer cell line ChIP-seq data II

Project description:T47D Breast cancer cell line ChIP-seq data II

| PRJNA454709 | ENA

Genome-Wide Progesterone Receptor Binding: Cell Type-Specific and Shared Mechanisms in Uterine Fibroids and Breast Cancer (ChIP-Seq)

Project description:Analysis of genes regulated by RU486 (an progesterone antagonist) in human breast cancer T47D cells and human uterine leiomyoma smooth muscle cells. The hypothesis is that RU486 inhibits tumor growth by inactivating the transcription of multiple genes which trigger critical signaling pathways to induce tumorigenesis in both breast caner and uterine leomyoma. Tissue-specific and common patterns of gene regulation may determine the therapeutic effects of antiprogestins in uterine leiomyoma and breast cancer. We applied ChIP-seq to identify PR-interaction sites in T47D breast cancer cells and primary uterine leiomyoma cells treated with RU486.

2012-09-11 | E-GEOD-40724 | biostudies-arrayexpress

RHBDD2 silencing and gene expression profiling of breast cancer cells

Project description:In previous studies, we identified a distantly related rhomboid homologue gene known as RHBDD2 (Rhomboid domain containing 2) to be markedly overexpressed in the advanced stages of the breast and colorectal cancer diseases. In order to identify RHBDD2 modulated pathways, we analyzed two breast cancer cell lines (MCF7 and T47D) from control and RHBDD2-siRNA transient gene silencing followed by gene expression profiling analysis using the whole genome Toray 3D-GeneTM Human Oligo Chip. Statistical analysis of the Toray's 3D gene expression profiling data identified 566 commonly differentially expressed genes in association to the RHBDD2 knockdown in both breast cancer cell lines. Among the statistically significant over-represented biological process, we found the apoptosis, cell cycle and response to DNA damage process related genes. In addition, categories of genes found in the ubiquitin-proteasome and oxidative phosphorylation were also highly enriched related genes in the commonly deregulated gene list. We further used a lentivirus-based system (shRNA-pLKO.1) for stable silencing of RHBDD2 mRNA in the T47D breast cancer cell line. Using a staurosporine-induced apoptosis model, we demonstrate that RHBDD2 abrogation resulted in an apoptosis-resistant phenotype of T47D breast cancer cell line. These data are in line with a recent study, suggesting that RHBDD2 expression could be up-modulated in response to 5FU-induced apoptosis in colorectal cancer cells. Taken together, these data suggest that RHBDD2 could be involved in the modulation of the programmed cell death in cancer cells. In order to analyze differential gene expression profiling of RHBDD2 silencing and control cells, total RNA was isolated from replicate experiments from two breast cancer cell lines (MCF7 and T47D) derived from the negative control-siRNA and the RHBDD2-siRNA treatments in duplicate experiments.

2013-04-10 | E-GEOD-43015 | biostudies-arrayexpress

ZBTB7A and KDM5 activity co-regulate NF-kB target gene expression and oxidative phosphorylation in triple negative breast cancer

Project description:We previously described that the KDM5B histone H3 lysine 4 (H3K4) demethylase is an oncogene in estrogen receptor-positive breast cancer. Here we report that KDM5A is amplified and overexpressed in basal breast tumors and is associated with chemotherapy resistance. Using CRISPR knockout viability screens -/+ KDM5 inhibition (KDM5i), we found that deletion of the ZBTB7A transcription factor and core SAGA complex sensitized to KDM5i, whereas knockout of RHO-GTPases led to resistance. ChIP-seq and RNA-seq analyses revealed colocalization of ZBTB7A and KDM5A/B at promoters with high H3K4me3 and dependence of KDM5A binding on ZBTB7A. ZBTB7A knockout altered transcriptional response to KDM5i specifically at NF-kB target genes, oxidative phosphorylation, and E2F-driven proliferation pathways. Our work furthers understanding of KDM5-mediated gene regulation in breast cancer and identified key pathways mediating sensitivity to KDM5i.

2024-04-02 | MSV000094452 | MassIVE

The ets transcription factor ELF5 suppresses the estrogen sensitive phenotype and contributes to antiestrogen resistance in luminal breast cancer. [human ChIP-Seq]

Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. ChIP-Seq using an antibody to ELF5, in T47D breast carcinoma cell lines

2012-12-27 | E-GEOD-31216 | biostudies-arrayexpress

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