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3D genome architecture in MCF10A cells in repsonse to DNA damage and ER stress

ABSTRACT: 3D genome architecture in MCF10A cells in repsonse to DNA damage and ER stress

PROVIDER: PRJNA1149005 | ENA |

REPOSITORIES: ENA

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3D genome architecture in MCF10A cells in repsonse to DNA damage and ER stress

Project description:The goal of this experiment was to assess changes in 3D chromatin structure in mammary gland epithelial cell line (MCF10A) response to chemical stimuli via etoposide (DNA damage) or tunicamycin (ER stress). Micro-C method with a comprehensive promoter capture panel was used to increase resolution using the proprietary approach of Cantata/Dovetail Genomics

2025-08-25 | GSE275042 | GEO

DNase-seq during MCF10A-ER-Src cell transformation

Project description:We performed DNase-seq to study the dynamic genome-wide chromatin accessibility during MCF10A-ER-Src cell transformation.

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ChIP-seq for histone modifications during MCF10A-ER-Src cell transformation

Project description:We performed ChIP-seq for histone modifications to map chromatin status and dynamics during MCF10A-ER-Src cell transformation.

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Project description:We performed RNA-seq to examine RNA expression profiles during MCF10A-ER-Src cell transformation and upon knockdowns of transcription factors

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Short and long read sequencing of human mammary epithelial MCF10a-Snail-ER cells after Epithelial-to-Mesenchymal Transition initiation

Project description:We cultured MCF10a-Snail-ER cells and induced EMT initiation with tamoxifen. A matched sequencing of their PolyA RNA was performed, using Illumina and direct RNA Oxford Nanopore sequencing technologies. Both generated datasets supported the development of hybrid bioinformatics tools.

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Analysis of MIZ1, MYC-ER and MYC-ERVD binding sites in MCF10A cells

Project description:Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli and this protects long-lived organisms from cancer development. How cells discriminate physiological from supra-physiological levels of Myc is largely unknown. Here we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-sequencing experiments show that oncogenic levels of Myc, but not of MycV394D, a point mutant that does not bind Miz1, recruit Miz1 to core promoters and enable binding of Myc/Miz1 complexes to low-affinity target sites, correlating with repression of a specific set of target genes. Repressed genes encode proteins involved in cell adhesion, migration and wound healing; their promoters are enriched for binding sites of the serum response (SRF) factor. Restoring SRF activity attenuates Myc-induced apoptosis in response to glutamine starvation, exposure to Trail and to DNA damage. We propose that supra-physiological levels of Myc engage Miz1 in repressive DNA binding complexes and suppress transcriptional progress. MIZ1, MYC-ER and MYC-ERVD ChIP-Seq with 10E2 and HC20 anti-ERalpha antibodies in MCF10A cells, performed on an Illumina IIx Genome Analyzer. Input sample is accessioned as GSM1423726.

2015-07-10 | E-GEOD-59146 | biostudies-arrayexpress

MYC-ER and MYC-ER V394D induced gene expression changes in MCF10A cells

Project description:Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli and this protects long-lived organisms from cancer development. How cells discriminate physiological from supra-physiological levels of Myc is largely unknown. Here we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-sequencing experiments show that oncogenic levels of Myc, but not of MycV394D, a point mutant that does not bind Miz1, recruit Miz1 to core promoters and enable binding of Myc/Miz1 complexes to low-affinity target sites, correlating with repression of a specific set of target genes. Repressed genes encode proteins involved in cell adhesion, migration and wound healing; their promoters are enriched for binding sites of the serum response (SRF) factor. Restoring SRF activity attenuates Myc-induced apoptosis in response to glutamine starvation, exposure to Trail and to DNA damage. We propose that supra-physiological levels of Myc engage Miz1 in repressive DNA binding complexes and suppress transcriptional progr 4 different experimental conditions were analyzed: MYC-ER 4-OHT treated versus MYC-ER ctr-treated (EtOH), MYC-ER V394D 4-OHT treated versus MYC-ER V394D ctr-treated; 3 biological replicates for every condition.

2015-07-10 | E-GEOD-59145 | biostudies-arrayexpress

ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

Project description:ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

2024-08-20 | PXD055020 |

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE24497: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1) GSE24499: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2) Refer to individual Series

2010-10-07 | E-GEOD-24500 | biostudies-arrayexpress

Expression profiling of MCF10A cells in 2D and 3D culture

Project description:In these microarray experiments, we characterize the gene expression of mammary epithelial cells (MCF10A cells) grown in either a traditional monolayer cell culture setting (2D) or on Matrigel, which induces single MCF10A cells to form organized acinar structures (3D). Morphogenesis of mammary epithelial cells into organized acinar structures in vitro is accompanied by widespread changes in gene expression patterns, including a substantial decrease in expression of Myc. The purpose of this study was to analyze the impact of morphogenesis and organization on gene expression with respect to changes in overall gene expression and Myc target gene expression. MCF10A cells were cultured in 2D for either 2 or 5 days (3 biological replicates each) or in 3D for 8 or 16 days (3 or 5 biological replicates, respectively)

2011-06-01 | E-GEOD-26148 | biostudies-arrayexpress

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