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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of E2F1 dependent gene expression in mouse testicular tissue

ABSTRACT: The effect of E2F1 loss on gene expression in testicular tissue was analyzed in 20-day old E2F1-/-, E2F1+/- mice. The hypothesis ws that there would be clear changes in expression of genes related to cell cycle machinery. The results show that E2F1 has wider implications in gene expression dynamics in testicular cell types than merely controlling cell cycle related genes. Total RNA obtained from testis tissue of 20-day-old E2F1-/- (KO), E2F1+/- (HZ) and E2F1+/+ mice (WT).

ORGANISM(S): Mus musculus

SUBMITTER: Emmi Rotgers

PROVIDER: E-GEOD-67989 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of E2F1 dependent gene expression in mouse testicular tissue

Project description:The effect of E2F1 loss on gene expression in testicular tissue was analyzed in 20-day old E2F1-/-, E2F1+/- mice. The hypothesis ws that there would be clear changes in expression of genes related to cell cycle machinery. The results show that E2F1 has wider implications in gene expression dynamics in testicular cell types than merely controlling cell cycle related genes.

2015-09-01 | GSE67989 | GEO

E2F1 ChIP-Seq on mouse hepatocytes overexpressing E2F1

Project description:E2F transcription factors are known regulators of the cell cycle, proliferation, apoptosis and differentiation. We reveal an essential role for E2F1 in liver through the regulation of glycolysis and lipogenesis. E2F1 deficiency leads to a decreased in glycolysis and de novo synthesis of fatty acids in hepatocytes. ChIP-Seq was performed to determine direct tagets of E2F1 in hepatocytes. We highlight that E2F1 directly binds the promoters of genes implicated in metabolic process and notably key lipogenic genes to control these pathways.

2015-12-01 | GSE74006 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.

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Expression level is a key determinant of E2F1-mediated cell fate

Project description:Purpose: dose response analysis of E2F1 target genes expression in flow-sorted fractions with increasing amounts of fluorescently labled E2F1 Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000. Results: different target genes have different E2F1 activation thresholds. Numerous proliferation-related target genes are induced already by the lowest E2F1-levels. Intermediate E2F1 levels induce cdk inhibitors, which might be responsible for cell cycle arrest. Finally, although some apoptotic E2F1 targets are induced already by low E2F1 levels, many key apoptotic genes require higher E2F1 levels for induction. Conclusions: induction of different cell fates by increasing E2F1 levels might pertain to differential affinities of the targets.

2017-08-22 | GSE93365 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary endothelial cells, there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induced endothelial dysfunctions including upregulation of cell cycle programming and paracrine effect, proliferative and anti-apoptotic phenotypes, impaired cellular junction and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was showed to mediate the SOX17 deficiency-induced EC dysfunction. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.

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Hes6 expression is controlled by c-Myc and the AR to promote E2F1 activity and poor outcome in castrate-resistant prostate cancer (E2F1 ChIP-seq)

Project description:Hes6 is a transcription co-factor that is associated with stem cell characteristics in neural tissue, but its role in cancer remains uncertain. Here we show that Hes6 is controlled by c-Myc and the AR and can drive castration resistance in xenografts of the androgen-dependent LNCaP prostate cancer cell line model. Hes6 activates a cell cycle enhancing transcriptional network that maintains tumour growth in the absence of circulating androgen but with maintained nuclear AR. We demonstrate interaction between E2F1, the AR and Hes6 and show the co-dependency of these factors in the castration-resistant setting. In the clinical setting, we have discovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which could be pharmacologically targeted. E2F1 ChIPseq on LNCaP cells.

2014-04-17 | E-GEOD-36614 | biostudies-arrayexpress

Expression data from lenses triply deficient for E2F1, E2F2, and E2F3 transcription factors

Project description:The E2F family consists of transcriptional repressors and activators that control cell proliferation. In the classic paradigm of cell cycle regulation, the three activators, E2F1, E2F2 and E2F3, are invariably depicted as the final components of a CDK/Rb signaling cascade that executes the transcriptional program necessary to commit cells to enter S phase. Unexpectedly, we find through analysis of Affymetrix expression array data that mature lens epithelial cells deficient for E2F1-3 fail to repress cell cycle-regulated genes (and other targets of E2F) and that this corresponds with subsequent apoptosis and cellular collapse in the lens. Murine lenses were collected at two stages of development for RNA extraction and hybridization on Affymetrix microarrays. Our aim was to determine key events that lead to cellular collapse of lenses triply deficient for E2F1, E2F2, and E2F3 in neonates.

2010-06-23 | E-GEOD-16533 | biostudies-arrayexpress

Expression data from lenses triply deficient for E2F1, E2F2, and E2F3 transcription factors

2010-06-10 | GSE16533 | GEO

LncRNA AGPG confers endocrine resistance in breast cancer by promoting E2F1 activity

Project description:Resistance to endocrine therapy represents a major threat to patients with estrogen receptor α positive (ERα+) breast cancer. The development of resistance is mainly through activating E2F signaling. However, the mechanisms that govern E2F1 activity in these resistant cells remain poorly understood. Here, we identify Actin Gamma 1 Pseudogene 25 (AGPG) as a lncRNA whose expression is driven by epigenomic activation of enhancer in endocrine resistant breast cancer cells. High expression of AGPG is associated with poor survival of ERα+ breast cancer, especially in patients receiving endocrine therapy. Stable knockdown and overexpression of AGPG demonstrate that AGPG promotes endocrine resistance, cell cycle progression, cell proliferation in vitro and in vivo. AGPG functions by direct binding purine rich element binding protein α (PURα), a transcription factor repressing E2F1 signaling and sensitized ERα+ breast cancer cells to endocrine therapy. Via binding to the region responsible for PURα/E2F1 interaction in PURα protein, AGPG releases E2F1 from PURα, leading to activation of E2F1 signaling in ERα+ breast cancer cells. Clinically, E2F1 target genes are strongly correlated with AGPG and PURα expression. Thus, our study reveals AGPG as a promising biomarker and potential therapeutic target in breast cancer.

2023-07-12 | GSE218130 | GEO

Expression data from U2OS ER-E2F1 cells after FOXO knockdown and E2F1 activation

Project description:Effect of FOXO knockdown on E2F1-mediated transcription

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