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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

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

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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.

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Project description:We sought to investigate the anticancer effects of the novel FOXM1 inhibitor, STL001 in a variety of human cancers from solid tumors including ovarian cancer, colorectal cancer, breast cancer, and prostate cancers. Here, the capacity of the novel compounds STL001 as FOXM1 inhibitor was verified in human cancer cell lines from solid tumors. Further, we showed here that FOXM1 inhibitor STL001 treatment resulted in sensitization of cancer cells to apoptotic death by multiple chemotherapeutic agents. STL001 was studied further to verify its direct target engagement with FOXM1. We have also provided Transcriptome-supported evidence that STL001 exhibits selectivity toward suppressing FOXM1-controlled regulatory pathways. This study verify and characterize a novel FOXM1 inhibitor STL001 that effectively antagonize FOXM1 activity and sensitize a variety of human cancer cells to traditionally used chemotherapy agents, and may be suitable for further clinical evaluation in targeting chemotherapy resistance human cancers.

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