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Genome-wide mapping of FOXM1 binding reveals co-binding with oestrogen receptor alpha in breast cancer cells (ChIP-seq)

ABSTRACT: The forkhead transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in cancer. Increased levels of FOXM1 are associated with both poor prognosis and oestrogen receptor (ERalpha) status in primary breast cancer. In this study, we map FOXM1 binding genome wide in both ERalpha-positive (MCF-7) and -negative (MDA-MB-231) breast cancer cells. We identify a common set of FOXM1 binding events at cell cycle-regulating genes, but in addition, in MCF-7 cells we find a high level of concordance with ERalpha-binding regions. FOXM1 binding at these co-binding sites is dependent on ERalpha binding, as depletion of ER protein levels reduced FOXM1 binding. FOXM1 interacts directly with both ERalpha co-activator CARM1 and is required for H3 arginine methylation at the ERalpha complex. Inhibition of FOXM1 activity with the ligand thiostrepton resulted in decreased FOXM1 binding at cca. 1400 sites genome wide and reduced expression of genes correlated with poor prognosis in ERalpha-positive tumour samples. These data demonstrate a novel role for the forkhead protein FOXM1 as an ERalpha cofactor and provide insight into the role of FOXM1 in ERalpha-positive breast cancer. The FOXM1-binding sites were mapped by ChIP-Seq in MCF-7 and MDA-MB-231 cells. Cells were treated either with thiostrepton, a FOXM1 inhibitor, or with DMSO (as control). Four replicates were performed in MCF7 cells and two replicates in MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Dario Beraldi

PROVIDER: E-GEOD-40762 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide mapping of FOXM1 binding reveals co-binding with oestrogen receptor alpha in breast cancer cells (expression)

Project description:The forkhead transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in cancer. Increased levels of FOXM1 are associated with both poor prognosis and oestrogen receptor (ERalpha) status in primary breast cancer. In this study, we map FOXM1 binding genome wide in both ERalpha-positive (MCF-7) and -negative (MDA-MB-231) breast cancer cells. We identify a common set of FOXM1 binding events at cell cycle-regulating genes, but in addition, in MCF-7 cells we find a high level of concordance with ERalpha-binding regions. FOXM1 binding at these co-binding sites is dependent on ERalpha binding, as depletion of ER protein levels reduced FOXM1 binding. FOXM1 interacts directly with both ERalpha co-activator CARM1 and is required for H3 arginine methylation at the ERalpha complex. Inhibition of FOXM1 activity with the ligand thiostrepton resulted in decreased FOXM1 binding at cca. 1400 sites genome wide and reduced expression of genes correlated with poor prognosis in ERalpha-positive tumour samples. These data demonstrate a novel role for the forkhead protein FOXM1 as an ERalpha cofactor and provide insight into the role of FOXM1 in ERalpha-positive breast cancer. MCF-7 cells were treated with either thiostrepton or DMSO for 6 hr. Each treatment was carried out in replicates of 6.

2013-01-07 | E-GEOD-40766 | biostudies-arrayexpress

Genome-wide mapping of FOXM1 binding reveals co-binding with oestrogen receptor alpha in breast cancer cells (expression)

2013-01-07 | GSE40766 | GEO

Genome-wide mapping of FOXM1 binding reveals co-binding with oestrogen receptor alpha in breast cancer cells (ChIP-seq)

2013-01-07 | GSE40762 | GEO

Genome-wide mapping of FOXM1 binding reveals co-binding with estrogen receptor alpha in breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-07 | E-GEOD-40767 | biostudies-arrayexpress

Genome-wide identification of PIF1-binding sites and direct-target genes of PIF1 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF1 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF1-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF1 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43283 | biostudies-arrayexpress

Genome-wide identification of PIF4-binding sites and direct-target genes of PIF4 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF4, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF4 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Three biological replicates data of PIF4-binding sites were collected by comparing the parallel ChIP samples from Myc-epitope-tagged-PIF4 (P1M) overexpressing transgenic seedlings and the wild-type (WT) control.

2014-10-02 | E-GEOD-43284 | biostudies-arrayexpress

Genome-wide mapping of FOXM1 binding sites

Project description:There are nearly fifty forkhead (FOX) transcription factors encoded in the human genome and due to sharing a common DNA binding domain, they are all thought to bind to similar DNA sequences. It is therefore unclear how these transcription factors are targeted to specific chromatin regions to elicit specific biological effects. Here we used ChIP-seq to investigate the genome-wide chromatin binding mechanisms used by the forkhead transcription factor FOXM1. In keeping with its previous association with cell cycle control, we demonstrate that FOXM1 binds and regulates a group of genes which are mainly involved in controlling late cell cycle events in the G2 and M phases. However, rather than being recruited through canonical RYAAAYA forkhead binding motifs, FOXM1 binding is directed via CHR elements. FOXM1 binds these elements through protein-protein interactions with the MMB transcriptional activator complex. Thus, we have uncovered a novel and unexpected mode of chromatin binding of a FOX transcription factor which allows it to specifically control cell cycle-dependent gene expression. Examination of FOXM1 binding sites in G2/M U2OS cells

2012-11-05 | E-GEOD-38170 | biostudies-arrayexpress

Genome-wide identification of PIF3-binding sites and direct-target genes of PIF3 transcriptional regulation in skotomorphogenesis [ChIP-Seq]

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF3 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Four biological replicates data of PIF3-binding sites were collected by comparing the parallel ChIP samples from transgenic seedlings overexpressing Myc-epitope-tagged PIF3 (35S:PIF3-5xMyc, P3M) in pif3-3 null mutant background and the wild-type (WT) control.

2013-02-01 | E-GEOD-39215 | biostudies-arrayexpress

RGA binding sites in Arabidopsis thaliana seedlings

Project description:DELLA proteins act as hubs that relay environmental information to the multiple transcriptional circuits that control growth and development through physical interaction with transcription factors from different families. We have analyzed the presence of one DELLA protein at the Arabidopsis genome by chromatin immunoprecipitation coupled to large-scale sequencing and we find that it binds at the promoters of multiple genes. Enrichment analysis shows a strong preference for cis elements recognized by specific transcription factor families. In particular, we demonstrate that DELLA proteins are recruited by type-B ARABIDOPSIS RESPONSE REGULATORS (ARR) to the promoters of cytokinin-regulated genes, where they act as transcriptional co-activators. The biological relevance of this mechanism is underpinned by the necessity of simultaneous presence of DELLAs and ARRs to restrict root meristem growth and to promote photomorphogenesis. Provided are 3 biological replicates analysing RGA binding sites in Arabidopsis seedlings. ChIP-seq was performed on plants expressing RGA-GFP under the native RGA promoter and on non-transgenic control plants as reference

2015-07-23 | E-GEOD-59187 | biostudies-arrayexpress

Cellular reprogramming by the conjoint action of ERalpha, FOXA1 and GATA3 to a ligand-inducible growth state

Project description:Despite the role of the estrogen receptor alpha (ERalpha) pathway as a key growth driver for breast cells, the phenotypic consequence of exogenous introduction of ERalpha into ERalpha-negative cells paradoxically has been growth inhibition. We map the binding profiles of ERalpha and its interacting transcription factors (TFs), FOXA1 and GATA3, in MCF-7 breast carcinoma cells. We observe that these three TFs form a functional enhanceosome and cooperatively modulate the transcriptional networks previously ascribed to ERalpha alone. We demonstrate that these enhanceosome-occupied sites are associated with optimal enhancer characteristics with highest p300 coactivator recruitment, RNA Pol II occupancy, and chromatin opening. The enhancesome binding sites appear to regulate the genes driving core ERalpha function. Most importantly, we show that transfection of all three TFs was necessary to reprogram the ERalpha-negative MDA-MB-231 and BT-459 cells to restore the estrogen responsive growth and to transcriptionally resemble the estrogen-treated ERalpha-positive MCF-7 cells. Cumulatively, these results suggest that all of the enhanceosome components comprising ERalpha, FOXA1 and GATA3 are necessary for the full repertoire of the cancer-associated effects of the ERalpha. The analysis of ERalpha, FOXA1, and GATA3 in MCF-7 cancer cells was done by ChIP-seq data obtained either with estradiol (E2) stimulation or without stimulation using vehicle as a control. Using the ERalpha bindings defined by ChIP-seq (GSE23893), FOXA1 bindings (GSE26831), and GATA3 bindings (this Series), we analyzed the enhanceosome effect of the overlapped binding sites from ERalpha, FOXA1 and GATA3.

2011-09-05 | E-GEOD-29073 | biostudies-arrayexpress

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