Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of PFKFB4 deletion on transcriptional reprogramming in breast cancer cells

ABSTRACT: Effects of PFKFB4 deletion on transcriptional reprogramming in breast cancer cells

PROVIDER: PRJNA896994 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22148700.fastq.gz	Fastqsanger.gz
	SRR22148701.fastq.gz	Fastqsanger.gz
	SRR22148702.fastq.gz	Fastqsanger.gz
	SRR22148703.fastq.gz	Fastqsanger.gz
	SRR22148704.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Transcriptional effects of KLF15 deletion in soleus muscle

Project description:Transcriptional effects of KLF15 deletion in soleus muscle

| PRJNA674632 | ENA

Transcriptional effects of KLF15 deletion in quadriceps muscle

Project description:Transcriptional effects of KLF15 deletion in quadriceps muscle

| PRJNA674758 | ENA

Effects of PFKFB4 deletion on transcriptional reprogramming in breast cancer cells

Project description:To explore the mechanisms by which PFKFB4 promotes breast cancer metastasis, we CRISPR-Cas knock-out PFKFB4 in two breast cancer lines for RNA-seq to identify downstream target genes that are regulated by PFKFB4

2022-12-31 | GSE217132 | GEO

Transcriptional effects of the IWR1 deletion

2009-10-13 | GSE17303 | GEO

Coordinate Enhancer Reprogramming by GATA3 and AP1 Promotes Phenotypic Plasticity to Achieve Breast Cancer Endocrine Resistance

Project description:Phenotypic plasticity has emerged as an important mechanism of therapy resistance in cancers, yet the underlying molecular mechanisms remain unclear. Using an established breast cancer cellular model for endocrine resistance, we show that hormone resistance is associated with enhanced phenotypic plasticity, indicated by a general downregulation of luminal/epithelial differentiation markers and upregulation of basal/mesenchymal invasive markers. Our extensive omics studies, including GRO-seq on enhancer landscapes, demonstrate that the global enhancer gain/loss reprogramming driven by the differential interactions between ER-alpha and other oncogenic transcription factors (TFs), predominantly GATA3 and AP1, profoundly alters breast cancer transcriptional programs. Our functional studies in multiple biological systems support a coordinate role of GATA3 and AP1 in enhancer reprogramming that drives phenotypic plasticity to achieve endocrine resistance or cancer invasive progression. Thus, changes in TF-TF and TF-enhancer interactions can lead to genome-wide enhancer reprogramming, resulting in transcriptional dysregulations that promote plasticity and cancer therapy-resistance progression

2019-05-24 | MSV000083857 | MassIVE

FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer

Project description:FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer

| PRJNA512997 | ENA

Transcriptional effects of the IWR1 deletion

Project description:Analysis of the genome-wide transcrptional effects caused by the deletion of the IWR1 gene by comparing the transcriptional profile of a iwr1 mutant strain with the isogenic wild type strain when cells were exponentially grown in YPD medium. Three independent cultures for the wt and the iwr1 mutant were used for the whole genome transcription analysis and they were grown in YPD at the early exponential phase. Total RNA was isolated and cDNA synthesis and labeling, filter hybridization and quantification/normalization of hybridization signals were performed as described in Garcia-Martinez, J., Aranda, A. and Perez-Ortin, J.E. (2004) Mol Cell 15(2),303-313.

2009-10-13 | E-GEOD-17303 | biostudies-arrayexpress

Transcriptional response to interferon beta and effects of deletion of a predicted enhancer

Project description:Transcriptional response to interferon beta and effects of deletion of a predicted enhancer

| PRJNA937684 | ENA

FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer [ChIP-seq]

Project description:Forkhead box A1 (FOXA1) is a pioneer factor that facilitates chromatin binding and function of lineage-specific and oncogenic transcription factors. Here, we have demonstrated that FOXA1 overexpression in estrogen receptor-positive breast cancer cells drives genome-wide enhancer reprogramming to activate pro-metastatic transcriptional programs. Specifically, FOXA1 overexpression generated more gained chromatin binding regions than the lost regions with decreased FOXA1 binding. Furthermore, FOXA1 overexpression led to establishment of more gained enhancers marked with increased H3K27ac and/or H3K4me1 than the lost enhancers with decreased signals of these two histone marks. In addition, these altered enhancers were highly coordinated with FOXA1-chromatin binding (cistrome) and the alteration of transcriptome due to FOXA1 overexpression, suggesting the direct engagement of high FOXA1 in enhancer reprogramming. The coordination between FOXA1 cistrome, enhancer reprogramming, and transcriptome also exists in the tamoxifen-resistant MCF7 cell model with endogenous FOXA1 gene amplification. Overall, our study supports the notion that FOXA1 overexpression promotes enhancer reprogramming in ER-positive breast cancer to activate gene expression associated with endocrine resistance and metastasis.

2019-12-18 | GSE124654 | GEO

FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer [RNA-seq]

Project description:Forkhead box A1 (FOXA1) is a pioneer factor that facilitates chromatin binding and function of lineage-specific and oncogenic transcription factors. Here, we have demonstrated that FOXA1 overexpression in estrogen receptor-positive breast cancer cells drives genome-wide enhancer reprogramming to activate pro-metastatic transcriptional programs. We have identified the hypoxia-inducible transcription factor HIF-2α as the top FOXA1-engaged super-enhancer target induced by FOXA1 overexpression, activating pro-metastatic gene signatures associated with poor breast cancer outcome. Using two different siRNA sequences, we identified 917 and 1,107 genes commonly down- and up-regulated (FDR < 0.05), respectively, upon HIF-2α knockdown in tamoxifen-resistant MCF7L cells. The enriched GO terms of the down-regulated genes were predominantly linked to tumor metastatic traits. GSEA showed that this HIF-2α-dependent gene set was significantly enriched in the transcriptomes of the TCGA ER+ breast tumors expressing high HIF-2α, but not high HIF-1α. We show the selective efficacy of a HIF-2α antagonist (PT2385), currently in clinical trial for renal cell carcinoma, in repressing migration and clonogenicity of endocrine-resistant breast cancer cells expressing high FOXA1. Our study suggests that targeting HIF-2α is a new approach blocking the aberrant transcriptional programs under high FOXA1-induced enhancer reprogramming in treating endocrine-resistant and metastatic breast cancer.

2019-12-18 | GSE124655 | 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