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Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs

ABSTRACT: Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs

PROVIDER: PRJNA885891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21772621_1.fastq.gz	Fastqsanger.gz
	SRR21772621_2.fastq.gz	Fastqsanger.gz
	SRR21772622_1.fastq.gz	Fastqsanger.gz
	SRR21772622_2.fastq.gz	Fastqsanger.gz
	SRR21772623_1.fastq.gz	Fastqsanger.gz

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Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs (NanoString)

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Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs (RNA-Seq)

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Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs (NanoString)

Project description:Estrogen receptor α (ER) mutations occur in up to 30% of metastatic ER-positive breast cancers. Recent data has shown that ER mutations impact the expression of thousands of genes not typically regulated by wildtype ER. While the majority of these altered genes can be explained by constant activity of mutant ER or genomic changes such as altered ER binding and chromatin accessibility, as much as 33% remain unexplained, indicating the potential for post-transcriptional effects. Here we explored the role of microRNAs in mutant ER-driven gene regulation and identified several microRNAs that are dysregulated in ER mutant cells. These differentially regulated microRNAs target a significant portion of mutant-specific genes involved in key cellular processes. When the activity of microRNAs is altered using mimics or inhibitors, significant changes are observed in gene expression and cellular proliferation related to mutant ER. An in-depth evaluation of miR-301b led us to discover an important role for PRKD3 in the proliferation of ER mutant cells. Our findings show that microRNAs contribute to mutant ER gene regulation and cellular effects in breast cancer cells.

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Project description:The Estrogen Receptor alpha (ERα) controls key cellular functions in hormone responsive breast cancer by assembling in large functional multiprotein complexes. ERα ligands are classified as agonists and antagonist, according to the response they elicit, thus the molecular characterization of the of ERα nuclear iteractome composition following estrogen and antiestrogen stimulation whose is needed to understand their effects on estrogen target tissues, in particular breast cancer. To this aim interaction proteomics coupled to mass spectrometry (MS) was applied to map the ERα nuclear interacting partners in MCF7 breast cancer cell nuclei following estrogen and antiestrogen stimuli.

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Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ChIP-seq]

Project description:Estrogen receptor alpha (ESR1) mutations have been identified in hormone therapy resistant breast cancer and primary endometrial cancer. Analyses in breast cancer suggests that mutant ESR1 exhibits estrogen independent activity. In endometrial cancer, ESR1 mutations are associated with worse outcomes and less obesity, however experimental investigation of these mutations has not been performed. Using a unique CRISPR/Cas9 strategy, we introduced the D538G mutation, a common endometrial cancer mutation that alters the ligand binding domain of ESR1, while epitope tagging the endogenous locus. We discovered estrogen-independent mutant ESR1 genomic binding that is significantly altered from wildtype ESR1. The D538G mutation impacted expression, including a large set of non-estrogen regulated genes, and chromatin accessibility, with most affected loci bound by mutant ESR1. Mutant ESR1 is unique from constitutive ESR1 activity as mutant-specific changes are not recapitulated with prolonged estrogen exposure. Overall, D538G mutant ESR1 confers estrogen-independent activity while causing additional regulatory changes in endometrial cancer cells that are distinct from breast cancer cells.

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Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [RNA-seq]

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Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer [ATAC-seq]

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Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs.

Project description:Estrogen receptor α (ER) mutations occur in up to 30% of metastatic ER-positive breast cancers. Recent data has shown that ER mutations impact the expression of thousands of genes not typically regulated by wildtype ER. While the majority of these altered genes can be explained by constant activity of mutant ER or genomic changes such as altered ER binding and chromatin accessibility, as much as 33% remain unexplained, indicating the potential for post-transcriptional effects. Here, we explored the role of microRNAs in mutant ER-driven gene regulation and identified several microRNAs that are dysregulated in ER mutant cells. These differentially regulated microRNAs target a significant portion of mutant-specific genes involved in key cellular processes. When the activity of microRNAs is altered using mimics or inhibitors, significant changes are observed in gene expression and cellular proliferation related to mutant ER. An in-depth evaluation of miR-301b led us to discover an important role for PRKD3 in the proliferation of ER mutant cells. Our findings show that microRNAs contribute to mutant ER gene regulation and cellular effects in breast cancer cells.

| S-EPMC10233889 | biostudies-literature

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