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FOXM1 Orchestrates a Global Methylation Signature that Mimics the Cancer Epigenome

ABSTRACT: Aberrant upregulation of a single oncogene FOXM1 in primary normal human oral epithelial cells orchestrated a cancer-like methylome landscape This study have identified a unique FOXM1-induced epigenetic signature which may have potentials as biomarkers for early oral cancer screening, diagnostic and/or therapeutic interventions

ORGANISM(S): Homo sapiens

PROVIDER: GSE31767 | GEO | 2012/04/19

SECONDARY ACCESSION(S): PRJNA145189

REPOSITORIES: GEO

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FOXM1 Orchestrates a Global Methylation Signature that Mimics the Cancer Epigenome

Project description:Aberrant upregulation of a single oncogene FOXM1 in primary normal human oral epithelial cells orchestrated a cancer-like methylome landscape This study have identified a unique FOXM1-induced epigenetic signature which may have potentials as biomarkers for early oral cancer screening, diagnostic and/or therapeutic interventions Comparisons of primary human normal oral keratinocytes transduced with either EGFP (control) or FOXM1B and a head and neck squamous cell carcinoma cell line SCC15

2012-04-18 | E-GEOD-31767 | biostudies-arrayexpress

FOXM1 in Early Human Squamous Cell Carcinoma Oncogenesis and it Is Enhanced by Nicotine during Malignant Transformation

Project description:Genome-wide SNP profilling for loss of heterozygosity (LOH) during FOXM1B-induced malignant transformation in a human premalignant oral keratinocyte line SVpgC2a. Keywords: oral cancer, keratinocytes, head and neck squamous cell carcinoma, FOXM1, genomic instability, SNP array, loss of heterozygosity, malignant transformation

2009-06-13 | GSE11782 | GEO

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [ChIP-Seq]

Project description:FOXM1 is a key transcription factor regulating cell cycle progression, DNA damage response, and a host of other hallmark cancer features, but the role of the FOXM1 cistrome in driving estrogen receptor-positive (ER+) vs. ER- breast cancer clinical outcomes remains undefined. Chromatin immunoprecipitation sequencing (ChIP-Seq) coupled with RNA sequencing (RNA-Seq) analyses was used to identify FOXM1 target genes in breast cancer cells (MCF-7) where FOXM1 expression was either induced by cell proliferation or repressed by p53 upregulation.

2015-10-26 | E-GEOD-72977 | biostudies-arrayexpress

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [RNA-Seq]

2015-10-26 | E-GEOD-73370 | biostudies-arrayexpress

Suppression of FOXM1 Activities and Breast Cancer Growth in Vitro and in Vivo by a New Class of Compounds

Project description:The transcription factor FOXM1 is up-regulated and overexpressed in aggressive, therapy-resistant forms of hormone receptor-positive and triple negative breast cancers, and is associated with less good patient survival. FOXM1 pathway signaling is also a key driver in other aggressive cancers, including those in prostate, lung, ovary, and gastrointestinal tract. Therefore, our goal has been to identify compounds effective in suppressing FOXM1 activity and breast cancer proliferation, and displaying good potency and pharmacokinetic properties for in vivo antitumor efficacy. In this report, we describe our studies on the FOXM1 targeting activities of 1,1-diarylethylene mono- and diamine compounds and their methiodide salts in cell-free, cell-based, and in vivo assays. The compounds bind directly to FOXM1 and alter its proteolytic sensitivity, reduce the cellular level of FOXM1 protein, and suppress the proliferation of breast cancer cells. RNA-seq and gene set enrichment analyses indicate that the compounds NB-73 and NB-55 decrease the expression of FOXM1-regulated genes and suppress gene ontology processes known to be under FOXM1 regulation. Several compounds with favorable pharmacokinetic properties were studied in preclinical breast tumor models. One compound (NB-55) had good oral efficacy in suppressing the growth of FOXM1-containing breast tumors in NOD-SCID-gamma (NSG) mice, and several others (NB-73, NB-115, and NB-63) had good efficacy in tumor growth suppression by subcutaneous administration. Our findings identify and characterize a new class of compounds that effectively antagonize FOXM1 actions and tumor growth that may be suitable for further clinical evaluation in targeting aggressive breast cancers driven by FOXM1.

2019-12-10 | GSE132343 | GEO

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [RNA-Seq]

2015-10-26 | GSE73370 | GEO

FOXM1 Cistrome Predicts Breast Cancer Metastatic Outcome Better Than FOXM1 Expression Levels or Tumor Proliferation Index [ChIP-Seq]

2015-10-26 | GSE72977 | GEO

FoxM1-Retinoblastoma Interaction Induces Tumor Microenvironment That Drives Metastasis

Project description:A mouse strain expressing an Rb-binding deficient mutant of FoxM1, FoxM1 DD, develops PyMT-driven mammary tumors that are deficient in metastasis. Single-cell RNA-Seq analyses revealed altered tumor microenvironment (TME). Unlike the FoxM1 +/+ tumors, the FoxM1 DD/DD tumors lack tumor-infiltrating cells, resulting from a deficiency in the tumor cell-populations that express factors necessary for their recruitment. Furthermore, FoxM1 DD/DD tumors contain fewer mammary cancer stem/progenitor cells, but more differentiated tumor cells.

2024-06-20 | GSE178612 | GEO

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 (ChIP-seq)

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

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