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Conserved and dynamic ESR1 signaling in developing cortex mediates early postnatal social behavior [snATAC-seq]

ABSTRACT: To dissect the genomic function of Esr1 in neonatal cortical neurons, we performed estradiol benzoate or vehicle treatment on P1 Esr1-Cre;LSL-Sun1-GFP animals and harvested the neocortex to perform single-nucleus assay for transposase-accessible chromatin using sequencing (snATAC-seq) with the GFP+ cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE277917 | GEO | 2025/09/29

REPOSITORIES: GEO

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Conserved and dynamic ESR1 signaling in developing cortex mediates early postnatal social behavior [scRNA-seq]

Project description:To define the cell types expressing Esr1 in the developing mouse cortex, we applied scRNA-seq from P1 neocortex expressing the transgenic reporter. Droplet-based scRNA-seq was performed with both GFP+ (cellular lineages expressing Esr1) and unsorted, whole populations.

2025-09-29 | GSE277918 | GEO

Conserved and dynamic ESR1 signaling in developing cortex mediates early postnatal social behavior [snATAC-seq]

Project description:Conserved and dynamic ESR1 signaling in developing cortex mediates early postnatal social behavior [snATAC-seq]

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esr1-drn-Transcriptomic study of the transcription factor ESR1/DRN.

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Targeting kinome reprogramming in ESR1 fusion-driven metastatic breast cancer

Project description:Transcriptionally active ESR1 fusions promote endocrine therapy (ET)-resistant growth and metastasis of estrogen receptor-alpha positive (ERα+) breast cancer. Currently, there are no targeted treatment options for tumors harboring active fusions because the ESR1 ligand binding domain (LBD) has been replaced with non-drug binding sequences from the 3’ partner gene. A mass spectrometry (MS)-based Kinase Inhibitor Pulldown Assay (KIPA) demonstrated an increase of multiple receptor tyrosine kinases including RET in T47D cells expressing active ESR1 fusions. Integrated proteogenomics defined tumor subsets that could be responsive to RET and CDK4/6 directed therapy from 22 biologically heterogeneous ERα+ patient-derived xenograft (PDX) tumors. Inhibition of RET by repurposing an FDA-approved drug significantly suppressed ESR1 fusion-driven growth of cell, PDX-derived organoid (PDXO) and PDX models. CDK4/6 inhibitor treatment showed similar tumor reductions to RET inhibition. Here, we reveal therapeutic kinase vulnerabilities in ESR1 fusion-driven tumors, which will lay the framework for future clinical trials.

2023-10-24 | PXD033339 | Pride

Proteomic characterization of ESR1 mutant cells

Project description:Three quarters of all breast cancer cases express the estrogen receptor (ER, ESR1 gene), which promotes tumor growth and constitutes a direct target for endocrine therapies. ESR1 mutations have been implicated in therapy resistance in metastatic breast cancers, in particular to aromatase inhibitors. ESR1 mutations promote constitutive ER activity and affect other signaling pathways, allowing cancer cells to proliferate by employing mechanisms within and outwith direct regulation by the ER. Although subjected to extensive genetic and transcriptomic analyses, understanding of protein alterations remains poorly investigated. Towards this, we employed an integrated mass spectrometry (MS) based proteomic approach to profile the protein and phosphoprotein differences in breast cancer cell lines expressing the frequent Y537N and Y537S ER mutations. Global proteome analysis revealed enrichment of mitotic and immune signaling pathways in ER mutant cells, while phosphoprotein analysis evidenced enriched activity of proliferation associated kinases, in particular CDKs and MTOR. Integration of protein expression and phosphorylation data revealed pathway-dependent discrepancies (motility vs proliferation) that were observed at varying degrees across mutant and wt ER cells. Additionally, protein expression and phosphorylation patterns, while under different regulation, still recapitulated the estrogen-independent phenotype of ER mutant cells.

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