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Gene expression profile in E2F1 and E2F2 deficient mice treated with the procarcinogen agent diethylnitrosamine and fed a high fat diet

ABSTRACT: Gene expression profile in E2F1 and E2F2 deficient mice treated with the procarcinogen agent diethylnitrosamine and fed a high fat diet

PROVIDER: PRJNA482062 | ENA |

REPOSITORIES: ENA

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Gene expression profile in E2F1 and E2F2 deficient mice treated with the procarcinogen agent diethylnitrosamine and fed a high fat diet

Project description:To investigate mechanism involved in the development of NAFLD-driven hepatocarcinoma (HCC), we used genome microarray expression profiling. The aim was to identify genes which upregulation could be controlled by E2F1 and/or E2F2 in NAFLD -driven HCC. For that, HCC was induced in wild type (WT), E2f1 knockout mice (E2f1-/-) and E2f2 knockout mice (E2f2-/-) by administration of the procarcinogenic agent diethylnitrosamine (DEN) combined with a feeding of high fat diet (HFD) for 32 weeks.The microarray results were then validated by RT-qPCR. For that, the expression of the selected genes (some overexpressed, some downregulated and others with no change) was measured in the same RNA samples by real time PCR. The results were clustered in pathways with the Reactome Database.

2021-03-26 | GSE117420 | GEO

siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells

Project description:To study the effect of siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells.

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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

E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

Project description:This SuperSeries is composed of the following subset Series: GSE32353: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter) GSE32354: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix) Refer to individual Series

2012-08-31 | E-GEOD-32355 | biostudies-arrayexpress

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

2010-06-10 | GSE16533 | GEO

siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells

Project description:siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells

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Analysis of E2F2 interacting proteins

Project description:In an attempt to identify proteins interacting with transcription factor E2F2, proteins extracted from HA-E2F2 overexpressing HEK293T cells were were subjected to immunoprecipitation (IP) with an anti-HA antibody or, as a negative control (NegCt), with an anti-T antibody. Immunoprecipitated proteins were eluted, digested with trypsin, and the resulting peptides were analyzed by LC-MS/MS. The whole procedure was repeated several times in an attempt to gauge reproducibility (nine replicates of the anti-HA IP and six replicates of the control IP).

2013-01-18 | PXD000026 | Pride

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

ChIP-chip from lymph node-derived primary lymphocytes with anti-E2F2 and anti-SV40TAg

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Increased metastasis with loss of E2F2 in Myc-driven tumors

Project description:In human breast cancer, mortality is associated with metastasis to distant sites. Therefore, it is critical to elucidate the biological mechanisms that underlie tumor progression and metastasis. Using signaling pathway signatures we previously predicted a role for E2F transcription factors in Myc induced tumors. To test this role we interbred MMTV-Myc transgenic mice with E2F knockouts. Surprisingly, we observed that the loss of E2F2 sharply increased the percentage of lung metastasis in MMTV-Myc transgenic mice. Examining the gene expression profile from these tumors, we identified genetic components that were potentially involved in mediating metastasis. These genes were filtered to uncover the genes involved in metastasis that also impacted distant metastasis free survival in human breast cancer. In order to elucidate the mechanism by which E2F2 loss enhanced metastasis we generated knockdowns of E2F2 in MDA-MB-231 cells and observed increased migration in vitro and increased lung colonization in vivo. We then examined genes that were differentially regulated between tumors from MMTV-Myc, MMTV-Myc E2F2-/-, and lung metastases samples and identified PTPRD. To test the role of PTPRD in E2F2-mediated breast cancer metastasis, we generated a knockdown of PTPRD in MDA-MB-231 cells. We noted that decreased levels of PTPRD resulted in decreased migration in vitro and decreased lung colonization in vivo. Taken together, these data indicate that E2F2 loss results in increased metastasis in breast cancer, potentially functioning through a PTPRD dependent mechanism.

2016-08-08 | GSE71815 | GEO

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