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Identification of Nrg1 enhancer binding proteins

ABSTRACT: Hyperglycemia is a risk factor for breast cancer-related morbidity and mortality. Hyperglycemia induces Neuregulin 1 (Nrg1) overexpression in breast cancer, which subsequently promotes tumor progression. However, molecular mechanisms underlying hyperglycemia-induced Nrg1 overexpression remain poorly understood. Here, We used DNA-protein pull-down using Nrg1 enhancer sequence as bait followed by LC/MS and identified RBPJ as a key component of the Nrg1 enhanceosome. We show that hyperglycemia causes active histone modifications at the Nrg1 enhancer, forming enhanceosome complexes where RBPJ, P300, and SETD1A are recruited to upregulate Nrg1 expression.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Epithelial Cell

DISEASE(S): Breast Cancer

SUBMITTER: Changhu Lee

LAB HEAD: Jiyoung Park

PROVIDER: PXD038668 | Pride | 2023-01-29

REPOSITORIES: Pride

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			Action	DRS
	1_2_3.sf3	Other
	Mudpit_01_L-12.mzid.gz	Mzid
	Mudpit_01_L-12.mzid.gz_Mudpit_01_L-12.MGF	Mzid
	Mudpit_02_L-12.mzid.gz	Mzid
	Mudpit_02_L-12.mzid.gz_Mudpit_02_L-12.MGF	Mzid

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Identification of Nrg1 enhancer binding proteins

Project description:Hyperglycemia is a risk factor for breast cancer-related morbidity and mortality. Hyperglycemia induces Neuregulin 1 (Nrg1) overexpression in breast cancer, which subsequently promotes tumor progression. However, molecular mechanisms underlying hyperglycemia-induced Nrg1 overexpression remain poorly understood. Here, We used DNA-protein pull-down using Nrg1 enhancer sequence as bait followed by LC/MS and identified RBPJ as a key component of the Nrg1 enhanceosome. We show that hyperglycemia causes active histone modifications at the Nrg1 enhancer, forming enhanceosome complexes where RBPJ, P300, and SETD1A are recruited to upregulate Nrg1 expression.

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The Neuregulin 1-HER axis as a key mediator of hyperglycemic memory effects in breast cancer

Project description:Poor outcomes in diabetic patients are observed across a range of human tumors, suggesting that cancer cells develop unique characteristics under diabetic conditions. Cancer cells exposed to hyperglycemic insults acquire permanent aggressive traits of tumor growth, even after a return to euglycemic conditions. Comparative genome-wide mapping of hyperglycemia-specific open chromatin regions and concomitant mRNA expression profiling revealed that neuregulin-1 gene, an established endogenous ligand for the HER3 receptor, is activated through a putative distal enhancer. Our findings highlight the targeted inhibition of NRG1-HER3 pathways as a potential target for the treatment breast cancer patients with associated diabetes Chromatin was extracted from hyperglycemic (HyG) and euglycemic (Control) cancer cells; FAIRE DNA and input DNA from each sample were used to generate libraries for single end sequencing on the the SOLiD 4 HQ system

2012-09-19 | E-GEOD-40949 | biostudies-arrayexpress

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Project description:The specificity of humoral immune responses depends on the functional rearrangement and expression of only one allele of immunoglobulin (Ig) genes. Here, we analyzed the comprehensive proteome of the murine Ig Emu enhancer, which governs the rearrangement and expression of the Ig mu heavy chain allele. By mass spectrometry of proteins bound at wild type versus mutant Emu enhancers, we identified Emu-binding proteins and associated multi-protein complexes. We found that the MSL/MOF complex, a regulator of gene dosage compensation in flies, binds Emu via transcription factor YY1 and facilitates Emu-driven chromatin looping and promoter interaction. Msl2 gene knockout in primary pre-B cells or Mof heterozygosity in mice reduced mu gene expression. In this data set we compare proteins binding to the wild-type Emu versus a DNA bait control for which the E1 box of the core enhancer region was mutated (E1mt).The E1mt abrogates binding of proteins recognizing the E1 box (e.g. YY1). Max LFQ quantitative proteomics was employed in an approach incubating wild-type and control DNA with (unlabeled) nuclear extracts.

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Enhancer bound proteome of intronic Ig Emu CORE enhancer with reverse DNA sequence polarity control bait

Project description:The specificity of humoral immune responses depends on the functional rearrangement and expression of only one allele of immunoglobulin (Ig) genes. Here, we analyzed the comprehensive proteome of the murine Ig Emu CORE enhancer, which governs the rearrangement and expression of the Ig mu heavy chain allele. The Ig Emu consists of a CORE enhancer (harboring a multitude of transcription factor binding sites) and two 5’ and 3’ flanking MAR (matrix attachment region) elements. By mass spectrometry of proteins bound at wild type versus mutant Emu enhancers, we identified Emu-binding proteins and associated multi-protein complexes. We found that the MSL/MOF complex, a regulator of gene dosage compensation in flies, binds Emu via transcription factor YY1 and facilitates Emu-driven chromatin looping and promoter interaction. Msl2 gene knockout in primary pre-B cells or Mof heterozygosity in mice reduced mu gene expression. In this data set we compare proteins binding to the wild-type Emu versus a DNA bait control for which the Emu CORE sequence was switched to its reverse polarity sequence (the flanking MARs sequence are wild-type). The latter conserves the DNA GC content but virtually destroys all sequence-specific transcription factor binding sites. Of note, DNA repetitive sequences that can also be bound by DNA interacting proteins are kept functional by this control bait. SILAC quantitative proteomics was employed in a label swap approach incubating wild-type and control DNA with labeled and non-labled protein extracts, respectively.

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Genome wide identification of enhancer regions in the retrosplenial cortex of the prairie vole, Microtus ochrogaster.

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