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ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

ABSTRACT: E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in SUM159 triple negative breast cancer cell line. Both input and immunoprecipitated DNA of two independant experiments were exhaustively sequenced and mapped on the human genome (hg38). Peak detection has been achieved with the HOMER suite algorithms.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128104 | GEO | 2022/03/01

REPOSITORIES: GEO

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ChIP-seq of E4F1 in primary mouse embryonic fibroblasts (MEFs) and in p53-/-, Ha-RasV12-transformed MEFs

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to decipher E4F1 cellular target genes, we performed chromatin immunoprecipitation of endogenous E4F1 in primary and in p53KO, Ha-RasV12-transformed MEFs. Both input and immunoprecipitated DNA were exhaustively sequenced and mapped on the mouse genome (mm9). Peak detection has been achieved by combining two peak calling algorithms. Intersection of the two E4F1 peak lists on each cell line were considered as E4F1 chromatin bound regions. Genome-wide mapping of E4F1 binding in mouse embryonic fibroblasts.

2015-04-01 | E-GEOD-57228 | biostudies-arrayexpress

ChIP-seq of E4F1 in mouse embryonic stem cells (mESCs)

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ChIP-seq of E4F1 in primary mouse embryonic fibroblasts (MEFs) and in p53-/-, Ha-RasV12-transformed MEFs

2015-04-01 | GSE57228 | GEO

RNA-seq of shE4F1 or shCTRL SUM159 triple negative breast cancer cell line treated or not with Gemcitabine

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Expression analysis of p53-/- and p53-/-, Ha-RasV12-transformed MEFs upon E4F1 gene inactivation

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Expression analysis of p53-/- and p53-/-, Ha-RasV12-transformed MEFs upon E4F1 gene inactivation

Project description:E4F1 is a ubiquitously expressed zinc-finger protein of the Gli-Kruppel family that was first identified, more than 30 years ago, as a cellular target of the adenoviral oncoprotein E1A13S (Ad type V), required for transcriptional regulation of adenoviral genes. In order to identify the p53-independent program controlled by E4F1, we performed microarray analyses in p53 KO and p53 KO; Ha-RasV12-transformed mouse embryonic fibroblasts (MEFs) in wild type and E4F1-inactivated cells. To address p53-independent E4F1 transcriptome, a 12 chip array study has been realized using total RNA recovered from wild-type (E4F1+/flox, CRE infected; odd Samples) MEFs and E4F1-depleted (E4F1-/flox, CRE infected; even Samples) MEFs in p53-/- (Samples 1 to 12) and p53-/-, Ha-RasV12 background (Samples 13 to 24). p53-/- MEFs were derived from 13.5-day mouse embryos. Transformed p53-/- MEFs were generated by infection with a recombinant retrovirus encoding for Ha-RasV12. Three independent biological replicates of wild-type and knock-out MEFs for E4F1 have been used on the two genetic backgrounds.

2015-04-01 | E-GEOD-57240 | biostudies-arrayexpress

ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

Project description:ChIP-seq of E4F1 in SUM159 triple negative breast cancer cell line

| PRJNA526474 | ENA

Spinophilin silencing in the breast cancer cell line SUM159

Project description:Microarray profiling was used to determine the most abundantly expressed genes in spinophilin-silenced breast cancer cells compared to control cells in the cell line SUM159. We identified several differentially expressed genes in spinophilin-silenced cells. A total number of six samples were analyzed, each in three replicates. There are three SUM159 Control samples and three samples of the cell line SUM159 with silenced spinophilin.

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ChIP-seq analysis of HN1L protein in SUM159 triple-negative breast cancer cells

Project description:Purpose: The goal of this study is to identify the role of HN1L protein as a transcription factor or co-factor in regulating TNBC cells. Methods: Due to the unavailability of a ChIP-grade HN1L antibody, we overexpressed FLAG-tagged HN1L in SUM159 cells and performed ChIP using anti-FLAG antibodies. ChIP DNA was prepared into libraries and sequenced by the Epigenomics Core of Weill Cornell Medical College using SR50 lane. Results: ChIP-Seq analysis began with mapping the sequenced reads to the genome. We utilized the Burrows-Wheeler Aligner (BWA) MEM algorithm to align the sequence reads against the human genome GRCh37/hg19 Assembly. We next used the Hypergoemetric Optimization of Motif Enrichment (HOMER) suite of tools to find and annotate peaks, and identify enriched motifs. HN1L showed 2,249 binding peaks from 10k bp upstream to 5k bp downstream of transcription start site (TSS). Conclusions: among the binding peaks 35 genes overlapped with a previously published BCSC gene signature, 10 genes overlapped with the HN1L knockdown gene signature and 8 genes are well established CSC transcription factors. When applying overlapped genes in the STRING10 pathway analysis database , a protein interaction network centered with STAT3 was obtained. STAT3 and FGFR2 peaks were validated by qPCR. Model-based Analysis of ChIP-Seq (MACS) was then used to confirm the peaks found by Hypergeometric Optimization of Motif EnRichment (HOMER) . Besides the binding peaks found in HOMER, another peak was called by MACS within LEPR , and was also validated by qPCR . These findings indicate that HN1L may act as a transcription factor through binding to enhancer regions of STAT3 and other STAT3 regulators.

2017-12-20 | GSE105446 | GEO

E4F1 coordinates pyruvate metabolism and the activity of the elongator complex to ensure protein translation fidelity during neuronal development

Project description:The Leigh syndrome is a severe inborn neurodegenerative encephalopathy that is commonly associated with pyruvate metabolism defects. The transcription factor E4F1, a key regulator of the pyruvate dehydrogenase complex (PDC), was previously found to be mutated in Leigh syndrome patients but the molecular mechanisms leading to cell death in E4F1-deficient neurons remain unknown. Here, we show that E4F1 coordinates a transcriptional program involved in AcetylCoenzyme A (AcCoA) production by the PDC and its utilization by the Elongator complex to acetylate tRNAs and thereby enhance protein translation fidelity in the central nervous system. E4F1 directly regulates the expression of Dlat and Elp3, two genes encoding key subunits of the PDC and the Elongator complex. Consistently, genetic inactivation of E4f1 in neurons during mouse embryonic development decreased the activity of the PDC and of the Elongator complex, resulting in impaired tRNAs editing and the induction of an endoplasmic reticulum (ER) stress / unfolded protein response (UPR) that led to neuronal cell death and microcephaly. Impaired expression of ELP3 and activation of an ATF-driven UPR response was also observed in fibroblasts from Leigh syndrome patients harboring a homozygous E4F1K144Q mutation. Our findings identify a novel crosstalk between pyruvate metabolism and the regulation of protein translation that is perturbed in Leigh syndrome patients.

2022-12-20 | GSE158595 | GEO

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