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Transcriptional regulation by Fra-1 in triple negative breast cancers

ABSTRACT: Transcriptional regulation by Fra-1 in triple negative breast cancers

PROVIDER: PRJNA612051 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11292321.fastq.gz	Fastqsanger.gz
	SRR11292322.fastq.gz	Fastqsanger.gz
	SRR11292323.fastq.gz	Fastqsanger.gz
	SRR11292324.fastq.gz	Fastqsanger.gz
	SRR11292325.fastq.gz	Fastqsanger.gz

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Transcriptional regulation by Fra-1 in triple negative breast cancers

Project description:This SuperSeries is composed of the SubSeries listed below. All the data are described in the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al.

2021-02-23 | GSE146825 | GEO

Blocking Fra-1 sensitizes triple-negative breast cancer to olaparib

Project description:Fra-1 (FOSL1) is overexpressed in triple-negative breast cancer (TNBC). Fra-1 is a member of the activator protein 1 (AP-1) transcription factor complex, which plays crucial roles in tumor progression and treatment resistance. We have previously identified 118 proteins that interact with endogenous chromatin-bound Fra-1 in TNBC cells in a large screen, and these included PARP1(Poly (ADP-ribose) polymerase 1). PARP1 inhibitor olaparib is currently in clinical use for treatment of BRCA-mutated TNBC breast cancer. Here, we demonstrate that this interaction impacts the efficacy of olaparib treatment. We corroborate that PARP1 interacts with Fra-1, and we show that PARP1 downregulates Fra-1 and consequently reduces AP-1 transcriptional activity. Inhibition of PARP1, on the other hand, increases Fra-1 levels and enhances its transcriptional activity, which in turn can increase treatment resistance. However, by inhibiting Fra-1, we found that TNBC cells became sensitized to olaparib treatment. We compared Fra-1 chromatin binding sites with the Fra-1 and PARP1 regulated transcriptomes, and found that a large fraction of PARP1-regulated genes was dependent on Fra-1. We further show that PARP1 protein levels significantly correlate with Fra-1 in clinical breast cancer tumors, and we identify that high PARP1 expression is indicative of a poor clinical outcome in breast cancer patients overall, but not in basal-like tumors. In conclusion, by exploring the functionality of the Fra-1 and PARP1 interaction, we propose that targeting Fra-1 could serve as a therapeutic approach to improve olaparib treatment outcome for TNBC patients.

2022-04-21 | GSE149621 | GEO

Blocking Fra-1 sensitizes triple-negative breast cancer to olaparib

Project description:Blocking Fra-1 sensitizes triple-negative breast cancer to olaparib

| PRJNA629373 | ENA

Identification of Fra-1 and/or Fra-2 regulated genes in MDA-MB231 cells

Project description:In the paper "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we identified Fra-1 and/or Fra-2 target genes in MDA-MB-231 cells. si RNA against Fra-1 and against Fra-2 were transfected in MDA-MB-231 cells either independenlty or simultaneously to identify genes regulated specifically by Fra-1 or Fra-2 and genes regulated redundantly or complementarily by Fra-1 and Fra-2 total RNA were purified and biotinylated sense-strand cDNA were produced. cDNA targets were used to probe Affymetrix GeneChip Human Gene 2.0 ST arrays

2021-02-23 | GSE146823 | GEO

NG-Capture C analysis of 35 gene loci regulated by Fra-1 in MDA-MB-231 cells

Project description:In the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we used NG Capture-C approach to identify regulatory elements interacting with the promoters of 35 Fra-1 regulated genes in the triple negative breast cancer cell line MDA-MB-231

2021-02-23 | GSE146824 | GEO

BRCAness, SLFN11 and RB1 loss predict response to topoisomerase I inhibitors in triple negative breast cancers

Project description:Expression data from patient-derived xenografts of human triple-negative breast cancers

2019-12-28 | GSE142639 | GEO

Comparative Characterization of 3D Chromatin Organization in Triple-Negative Breast Cancers

Project description:Comparative Characterization of 3D Chromatin Organization in Triple-Negative Breast Cancers

| PRJNA703390 | ENA

Transcriptomes of triple negative breast cancer enriched breast cancer cohort

Project description:Breast cancers enriched for the triple negative breast cancer phenotype with extensive clinico-pathological features were profiled to establish their comprehensive transcriptional profiles

2016-11-21 | E-MTAB-5270 | biostudies-arrayexpress

Insights into the invasiveness of triple negative breast cancer from genome-wide profiling of transcription factor AP-1 (expression)

Project description:Triple negative breast cancer (TNBC) is an aggressive clinical phenotype, and accounts for 15% to 20% of all breast cancers. The molecular determinants of malignant cell behaviors in TNBC remain largely unknown. We find that the AP-1 transcription factor component, Fra-1, is overexpressed in basal-like breast tumors, and its expression level has high prognostic significance. Depletion of Fra-1 or its heterodimeric partner c-Jun inhibits the proliferative and invasive phenotypes in TNBC cells. To gain insights into the transcriptional regulatory networks of AP-1 in TNBC cells, we combine genome-wide ChIP-seq with loss-of-function transcriptome analyses. We observe dysregulation of direct targets of the Fra-1/c-Jun heterodimer involved in cell proliferation, cell adhesion, and cell-cell contact. Intriguingly, we find that AP-1 mediates downregulation of E-cadherin through direct transcriptional induction of ZEB2. This work sheds light on the mechanisms and pathways by which TNBC acquires invasiveness and proliferative propensity. BT549 cells grown in complete medium were transfected with a control siRNA, siRNA targeting Fra-1 or siRNA targeting c-Jun for 72 h, and then global gene expression profiles were assessed. Three or four biological replicates were used for each group.

2014-06-30 | E-GEOD-46440 | biostudies-arrayexpress

Mapping of p300/CBP binding sites in MDA-MB-231 cells transfected with a control siRNA or a siRNA directed against Fra-1(FOSL1)

Project description:In the article "Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers" by Bejjani et al., we mapped p300/CBP binding sites in MDA-MB-231 cells transfected with a control siRNA or a siRNA directed against Fra-1(FOSL1) to study whether Fra-1 can modulate p300/CBP recruitment on MDA-MB-231 genome

2021-02-23 | GSE163304 | GEO

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