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EHF is an essential driver of mammary alveolar lineage differentiation and putative suppressor of breast tumorigenesis

ABSTRACT: EHF is an essential driver of mammary alveolar lineage differentiation and putative suppressor of breast tumorigenesis

PROVIDER: PRJNA915371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22881556.fastq.gz	Fastqsanger.gz
	SRR22881557.fastq.gz	Fastqsanger.gz

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EHF is an essential driver of mammary alveolar lineage differentiation and putative suppressor of breast tumorigenesis

Project description:The Ets homologous factor (Ehf) is highly expressed in the mammary gland in pregnancy and lactation. Mothers with Ehf deletion fail to lactate due to impaired lobuloalveolar development. scRNA-seq profiling of mammary epithelial cells (MECs) at late pregnancy (18.5dP) demonstrated that EhfKO mammary gland comprised fewer differentiated alveolar cells, and an accumulation of the preceding cell populations in the secretory differentiation hierarchy. EhfKO mammary alveolar cells also displayed significant downregulation of milk proteins and lipids, and increased expression of proliferation markers indicating incomplete differentiation

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EHF is an essential regulator of mammary alveolar lineage differentiation and putative suppressor of breast tumorigenesis

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Identification of genes differentially expressed between control and EHF siRNA transfected HCT116 cells

Project description:we found that EHF allowed colon tumor cells to escape p53-mediated apoptosis.We performed microarray analysis to find the target genes of EHF. A colorecal cancer cell line HCT116 was transfected with an siRNA targeting EHF or negative control.

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Expression data from siRNA knockdown of Ehf in primary human corneal epithelial cells

Project description:Ehf is a transcriptional regulator that is highly expressed and enriched in corneal epithelium. To gain insights into the role of Ehf in the corneal epithelium, we performed siRNA knockdown of Ehf in primary human corneal epithelial cells. Primary human corneal epithelial cells were transfected with siEhf or si controls, plated, and harvested at 72 hr.

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Coordinate regulation of ELF5 and EHF at the chr11p13 modifier region

Project description:E74-like factor 5 (ELF5) and ETS-homologous factor (EHF) are epithelial selective ETS family transcription factors (TFs) encoded by genes at chr11p13, a region associated with cystic fibrosis (CF) lung disease severity. EHF controls many key processes in lung epithelial function so its regulatory mechanisms are important. Using CRISPR/Cas9 technology, we removed three cis-regulatory elements (CREs) from the chr11p13 region in airway epithelial cells. Deletion of two enhancers and one CRE within a stretch enhancer at the EHF locus caused subtle changes in chromatin architecture, and though EHF expression did not change, ELF5 abundance increased. ELF5 is normally very low in airway cells so we next examined cell types that express more ELF5 (LNCaP and T47D). ATAC-seq experiments in these lines revealed novel peaks of open chromatin (potential CREs) at the 5’ end of chr11p13 that were associated with an expressed ELF5 gene. Furthermore, 4C-seq assays identified direct interactions between the active ELF5 promoter and sites within the EHF locus, suggesting coordinate regulation between these TFs. ChIP-seq for ELF5 in T47D cells revealed ELF5 occupancy within EHF introns 1 and 6 and siRNA-mediated depletion of ELF5 repressed EHF expression. These results define a new role for ELF5 in lung epithelial biology.

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