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Transcriptional regulation by Fra-1 in triple negative breast cancers

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146825 | GEO | 2021/02/23

REPOSITORIES: GEO

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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

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

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

Mapping of epigenetic marks (H3K4me1, H3K4me3, H3K27ac), p300/CBP, PolII and CTCF on MDA-MB-231 genome

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 epigenetic marks (H3K4me1, H3K4me3, H3K27ac), p300/CBP, PolII and CTCF to characterize the binding sites of Fra-1 and Fra-2 on MDA-MB-231 genome. Data for Fra-1 and Fra-2 ChIP-seq are available on GEO database, accession number GSE132098 (Tolza et al., 2019, MCR 17, 1999-2014)

2021-02-23 | GSE146822 | 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

Transcriptional regulation by Fra-1 in triple negative breast cancers

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

| PRJNA612051 | ENA

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

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

| PRJNA629373 | ENA

Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1

Project description:Fra-1, a member of the activator protein 1 (AP-1) family, is overexpressed in triple-negative breast cancer (TNBC) and plays crucial roles in tumor growth. Here we report the identification of 118 proteins interacting with endogenous chromatin-bound Fra-1 in TNBC cells, highlighting DDX5 as the most enriched Fra-1-interacting protein. DDX5, a previously unrecognized protein in the Fra-1 transcriptional network, shows extensive overlap with Fra-1 cistrome and transcriptome that are highly associated with the TNBC cell growth. We provide evidence that DDX5 expression enhances Fra-1 transcriptional activity and potentiates Fra-1-driven cell proliferation. Furthermore, we show that the DDX5 target gene signature predicts poor clinical outcome in breast cancer patients. DDX5 protein level was higher in triple-negative basal-like tumors than in non-basal-like tumors, including luminal A, luminal B, and HER2-enriched subtypes. Collectively, by combining proteomic and genomic approaches we reveal a role for DDX5 as a regulatory protein of Fra-1 signaling and suggest DDX5 as a potential therapeutic target for TNBC.

2019-09-03 | GSE112963 | GEO

Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1 [RNA-seq]

Project description:Fra-1, a member of the activator protein 1 (AP-1) family, is overexpressed in triple-negative breast cancer (TNBC) and plays crucial roles in tumor progression. However, a systematic analysis of the composition of the Fra-1 protein network specifically on chromatin is still missing. Here we performed endogenous purification of Fra-1 transcriptional complex under ChIP conditions, followed by mass spectrometry, to identify chromatin-bound partners of Fra-1 in TNBC cells. This study allowed the identification of 118 interactors, highlighting DDX5 as the high ranking of Fra-1 interacting proteins. DDX5, a previously unrecognized protein in the network, is recruited globally to Fra-1 binding sites and shares a substantial set of Fra-1 target genes required for the TNBC cell growth. We provide evidence that DDX5 expression enhances Fra-1 transcriptional activity, thereby enhancing Fra-1-driven tumorigenesis. By integrating ChIP-seq and RNA-seq, we show that DDX5 target gene signature predicts poor clinical outcome in breast cancer patients. DDX5 protein level was higher in triple-negative basal like tumors than in non-basal like tumors, including luminal A, luminal B and HER2-enriched subtypes. Collectively, this comprehensive Fra-1 interaction profiling provides a broad and deep view of Fra-1 chromatin interaction landscape, which will help in deciphering mechanisms of AP-1 regulation of gene expression.

2019-09-03 | GSE112962 | GEO

Endogenous interaction profiling identifies DDX5 as an oncogenic coactivator of transcription factor Fra-1 [ChIP-seq]

2019-09-03 | GSE112961 | GEO