Global enrichment of FoxM1 bound chromatin in Huh7 cell line
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA736049 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14760692.fastq.gz | Fastqsanger.gz | |||
| SRR14760693.fastq.gz | Fastqsanger.gz | |||
| SRR14760694.fastq.gz | Fastqsanger.gz |
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Project description:FoxM1 is an oncogenic transcription factor that has been linked to the genesis and progression of cancer. FoxM1 not only upregulates cell proliferation and survival genes, but also represses tumor suppressor genes according to our prior study. This ChIP-Seq is a part of our endeveavor to creat a map of the FoxM1 occupied chromatin area in order to better understand the FoxM1 role in tumorigenesis. We present the results of a high-throughput profile of Chromatine alteration in mammalian cells using ChIP-Seq. We developed genome-wide chromatin-state maps of the human HCC cell line Huh7 by extracting approximately 3 billion bases of sequence from chromatin immunoprecipitated DNA in approxiamtoly 33 million reads. We discovered that FoxM1 successfully distinguishes between expressed, stably repressed and poised genes and therefore reflect cell state and lineage potential. This research lays the groundwork for using extensive chromatin profiling to characterize the genes controlled by the oncogeneic transcription factor FoxM1 and their role in the development of FoxM1-induced cancers.
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Project description:FOXM1 is a vital transcription factor associated with proliferation, expressed extensively and dynamically throughout the cell cycle. Its overexpression in mycosis fungoides correlates with a poor prognosis. However, the specific role of FOXM1 in the pathogenesis of mycosis fungoides remains unclear. In this study, we silenced FOXM1 in the MyLa cell line, which is representative of mycosis fungoides, by transducing it with a lentivirus vector containing shRNA targeting the FOXM1 gene. By comparing MyLa cells transduced with scrambled shRNA as the control, we observed distinct gene expression profiles, notably a decrease in the expression of cell cycle-related genes and an increase in apoptosis-related genes. These changes align with the phenotypic alterations of MyLa cells following FOXM1 silencing.
2024-10-29 | GSE279807 | GEO
Project description:FoxM1, a mammalian Forkhead Box M1 protein, is known as a typical proliferation-associated transcription factor that regulates of G1/S and G2/M transition in the proliferating cells. However, the in vivo function of FoxM1 in adult stem cells remains unknown. Here, we found that FoxM1 is highly expressed in hematopoietic stem cells (HSCs) and is essential for maintaining quiescence and self-renewal of HSCs in vivo. FoxM1-deficient mice developed leukopenia, thrombocytopenia and neutropenia with an approximately 6-fold decrease in HSC pool size, which is associated with a failure of G0 cell cycle regulation and increased cell cycling in HSCs. FoxM1 absence did not affect lineage commitment of HSCs and progenitors. However, FoxM1 loss significantly reduced the repopulating capacity and self-renewal of long-term HSC in a cell-autonomous manner. Mechanistically, FoxM1 loss markedly down-regulates the expression of orphan nuclear receptor Nurr1, known to regulate HSC quiescence. We found that FoxM1 directly bound the promoter region of Nurr1 and induced transcriptional activity of Nurr1 promoter in vitro, and forced expression of Nurr1 rescued FoxM1-deletion-induced G0 loss of HSC-enriched population in vitro. Thus, our studies show a previously unrecognized role of FoxM1 as a critical regulator of HSC quiescence and self-renewal by controlling Nurr1-mediated pathways. The Hematopoietic Stem Cells (HSCs) were sorted from FoxM1[fl/fl] and Tie2-Cre FoxM1[fl/fl] mice, then amplified with Ovation Pico WTA System V2 before microarray analysis. There are 3 samples from FoxM1[fl/fl]mice and 3 samples from Tie2-Cre FoxM1[fl/fl] mice.
2015-06-15 | E-GEOD-62360 | biostudies-arrayexpress
Project description:Hep3B and Huh7 cells pre-treated with XL413 for 10 days to induce senescence prior to sertraline treatment for 24 hours. For RNA sequencing, the library was prepared using TruSeq RNA sample prep kit according to the manufacturer’s protocol (Illumina). Gene set enrichment analysis was performed using gene set enrichment analysis software.
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Project description:Chromatin immunoprecipitation using anti-FOXM1 (Santa Cruz Biotechnology: sc- 502X) antibodies in an OE33 cell line
2015-12-14 | E-MTAB-4121 | biostudies-arrayexpress
Project description:Purpose: To gain futher insight into how FOXM1 regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E15 FOXM1 conditional knock in mice and littermate wild-type. Methods: Total RNA from E15 telencephalic tissue of wild-type(WT) and FOXM1f/+;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and FOXM1f/+;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected human FOXM1 plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how FOXM1 gene contribute to brain cortical development.
2020-02-13 | GSE145169 | GEO
Project description:The Forkhead Box m1 (Foxm1 or Foxm1b) protein (previously called HFH-11B, Trident, Win, or MPP2) is abundantly expressed in human non-small cell lung cancers where it transcriptionally induces expression of genes essential for proliferation of tumor cells. In this study, we used Rosa26-Foxm1 transgenic mice, in which the Rosa26 promoter drives ubiquitous expression of Foxm1 transgene, to identify new signaling pathways regulated by Foxm1. Lung tumors in Rosa26-Foxm1 mice were induced using the 3-methylcholanthrene (MCA)/ butylated hydroxytoluene (BHT) lung tumor initiation/ promotion protocol. MCA/BHT-treated Rosa26-Foxm1 mice displayed a significant increase in the proliferation of lung tumor cells as well as in the number and size of lung adenomas. Elevated tumor formation in Rosa26-Foxm1 transgenic lungs was associated with persistent pulmonary inflammation, macrophage infiltration and increased expression of Cdc25C phosphatase, cyclin E2, chemokine ligands Cxcl5, Cxcl1 and Ccl3, cathepsins, and Matrix metalloprotease 12, all of which stimulate signaling pathways essential for cellular proliferation, pulmonary inflammation and remodeling. Lung tumors from Rosa26-Foxm1 mice displayed increased expression of Cyclooxygenase-2 (Cox-2), whereas diminished Cox-2 levels were observed in Foxm1-deficient lung tumors from Mx-Cre Foxm1 fl/fl mice. Cell culture experiments with A549 human lung adenocarcinoma cells demonstrated that depletion of Foxm1 by either siRNA transfection or treatment with Foxm1-inhibiting ARF 26-44 peptide significantly reduced Cox-2 expression. Foxm1 protein bound to the –3479/–3461 and –7826/–7795 bp regions of the human Cox-2 promoter, indicating that the human Cox-2 gene is a direct transcriptional target of Foxm1 in lung tumor cells. Keywords: Influence of genetic modification to the tumor development
2007-09-28 | GSE6641 | GEO
Project description:The Wnt signaling pathway is involved in many differentiation events during embryonic development and can lead to tumor formation after aberrant activation of its components. Β-catenin, a cytoplasmic component, plays a major role in the transduction of the canonical wnt/ β-catenin signaling. The aim of this study was to identify novel genes that are regulated by active β-catenin/TCF signaling in hepatocellular carcinoma. We selected and expanded isogenic clones from hepatocellular carcinoma-derived Huh7 cells with high and low β-catenin/TCF activities. We showed that, high TCF activity Huh7 cells lead to bigger and more aggressive tumors when xenografted into nude mice. We used SAGE (Serial Analysis of Gene Expression), genome-wide microarray and in silico promoter analysis in parallel, to compare gene expression between low (basal) and high (transfected) β-catenin/TCF activity clones, those had been xenografted into nude mice. We compared and contrasted SAGE and genome-wide microarray data, in parallel. Finally; after combined analysis, we identified BRI3 and HSF2 as novel targets of Wnt/β-catenin signaling in hepatocellular carcinoma. Experiment Overall Design: High TCF activity Huh7 cell line (Huh7-S33Y) was compared to control Huh7 cell line (Huh7-Vec) by using 10 ug of total RNA isolated from each sample (15 ug of labeled cRNA was hybridized to the arrays). Triplicates are coming from same total RNA extraction.
2009-10-10 | E-GEOD-11916 | biostudies-arrayexpress