Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167358 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR500261.fastq.gz | Fastqsanger.gz | |||
| SRR500262.fastq.gz | Fastqsanger.gz | |||
| SRR500263.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
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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. 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.
2013-01-07 | E-GEOD-40762 | biostudies-arrayexpress
Project description:The Forkhead transcription factor, FOXM1, is a key regulator of the cell cycle and is over-expressed in most types of cancer. FOXM1, similar to other Forkhead (FKH) factors binds to a canonical FKH motif in vitro. However, genome-wide mapping studies in different cell lines have shown a lack of enrichment of the FKH motif at FOXM1 binding sites suggesting an alternative mode of chromatin recruitment. We have investigated the role of direct versus indirect DNA binding in FOXM1 recruitment by performing ChIP-seq with WT and DNA binding deficient FOXM1. An in vitro fluorescence polarization (FP) assay was used to identify point mutations in the DNA binding domain (DBD) of FOXM1 that inhibit binding to a FKH consensus sequence. Stable cell lines expressing either WT or DBD mutant green fluorescence protein (GFP)-tagged FOXM1 were utilized for genome-wide mapping studies comparing the distribution of the DBD mutant protein to the WT. This showed that interaction of the DBD of FOXM1 with target DNA is essential for recruitment. Moreover, analysis of protein interactome of the WT versus DBD mutant FOXM1 showed that the reduced recruitment is not due to the mutation inhibiting protein-protein interactions. This study showed that a functional DBD domain is essential for FOXM1 chromatin recruitment. Even in FOXM1 mutants that show almost complete loss of binding the protein-protein interactome and pattern of phosphorylation are largely unaffected. These results strongly support a model whereby FOXM1 is specifically recruited to chromatin through co-factor interactions by binding directly to both canonical and non-canonical DNA sequences.
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