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ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [ChIP-Seq]

ABSTRACT: ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [ChIP-Seq]

PROVIDER: PRJNA525658 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8669850.fastq.gz	Fastqsanger.gz
	SRR8669851.fastq.gz	Fastqsanger.gz
	SRR8669852.fastq.gz	Fastqsanger.gz
	SRR8669853.fastq.gz	Fastqsanger.gz
	SRR8669854.fastq.gz	Fastqsanger.gz

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ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice

Project description:ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice

| PRJNA525654 | ENA

ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [RNA-Seq]

Project description:About 75% of all breast cancers express the nuclear hormone receptor oestrogen receptor α (ERα). However, the majority of mammary tumors from genetically engineered mouse models are ERα-negative. To model ERα-positive breast cancer in mice, we exogenously introduced expression of mouse and human ERα in an existing p53-deficiency driven breast cancer mouse model. After initial ERα expression during development of the mammary gland, expression was reduced or lost in adult glands and p53-deficient mammary tumors. ChIP-sequencing analysis of primary mouse mammary epithelial cells (MMECs) derived from these models, in which expression of the ERα constructs was induced in vitro, confirmed interaction of ERα with the DNA. In human breast and endometrial cancer, the pioneer factor FOXA1 is known to be essential to facilitate ERα/DNA binding. Surprisingly, the ERα binding sites identified in primary MMECs, but also in mouse mammary gland and uterus, showed a high enrichment of ERE motifs, but were devoid of Forkhead motifs. Furthermore, exogenous introduction of FOXA1 and GATA3 in ERα-expressing MMECs was not sufficient to promote ERα-responsiveness of these cells. Together, this suggests that species-specific differences in ERα-cistromes between mouse and human are dictated by the DNA sequence, resulting in ERα-dependencies in mice that are not FOXA1 driven and potentially not tumorigenic. These species-specific differences in ERα-biology can limit the use of mouse models in ERα-positive breast cancer research.

2019-11-13 | GSE127862 | GEO

ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [ChIP-Seq]

2019-11-13 | GSE127859 | GEO

ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [RNA-Seq]

Project description:ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice [RNA-Seq]

| PRJNA525659 | ENA

Estrogen receptor alpha ChIP-seq in p53 null mouse mammary gland

Project description:ERα is a major driver for breast cancer initiation and progression.However,the fundamental mechanisms,including global cistromic and genomic transcriptional responses that are required to elicit breast cancer initiation and progression in response to ERα, have not been elucidated. We used chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) to identify estrogen regulated genes that directly recruit ERα in the p53 null mouse mammary gland

2022-02-06 | GSE77977 | GEO

ERα over-expression does not accelerate development of p53-deficient mammary tumors in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-11-13 | GSE127863 | GEO

Expression data comparing Rb/p53 and p53 deficient mammary tumors and normal mammary tissue

Project description:To investigate the impact of combined Rb and p53 loss in mammary tumorigenesis, we used transgenic and viral approaches to delete Rb and p53 floxed alleles specifically in the mouse mammary epithelium. Although MMTV-Cre (NLST) targets stem/bi-potent progenitors in the mammary gland, a subset of MMTV-Cre:Rbf/f;p53f/f mice developed non-mammary tumors. Thus, freshly isolated primary mammary epithelial cells from these animals were transplanted into the mammary fat pads of immunodeficient mice and monitored for tumor formation. In addition, primary MECs were isolated from Cre-negative Rbf/f;p53f/f mice, infected with Ad-Cre followed by orthotopic transplantation. In all these cases, resulting tumors shared similar spindle-shape histology, expressed high levels of vimentin, a mesenchymal marker, but not E-cadherin, a luminal marker, and were classified as adeno-sacrcomatoid/spindle-cell/mesenchymal-like breast cancer. We used microarrays to detect differentially expressed genes in the Rb/p53 double-knock-out vs p53 single deletion or normal mammary tissue.

2014-10-03 | GSE62016 | GEO

Expression data comparing Rb/p53 and p53 deficient mammary tumors and normal mammary tissue

2014-10-03 | E-GEOD-62016 | biostudies-arrayexpress

Differential Roles of ERα and ERβ in Normal and Neoplastic Development in the Mouse Mammary Gland

Project description:The present experiments were performed to determine the roles of estrogen receptors α and β (ERα and ERβ) in normal and neoplastic development in the mouse mammary gland. In wild-type mice, in vivo administration of estradiol (E) + progesterone (P) stimulated mammary ductal growth and alveolar differentiation. Mammary glands from mice in which the ERβ gene has been deleted (βERKO mice) demonstrated normal ductal growth and differentiation in response to E + P. By contrast, mammary glands from mice in which the ERα gene has been deleted (αERKO mice) demonstrated only rudimentary ductal structures that did not differentiate in response to E + P. EGF demonstrates estrogen-like activity in the mammary glands of αERKO mice: treatment of αERKO mice with EGF + P (without E) supported normal mammary gland development, induced expression of progesterone receptor (PR), and increased levels of G- protein-coupled receptor (GPR30) protein. Mammary gland development in βERKO mice treated with EGF + P was comparable to that of wild-type mice receiving EGF + P; EGF had no statistically significant effects on the induction of PR or expression of GPR30 in mammary glands harvested from either wild-type mice or βERKO mice. In vitro exposure of mammary glands to 7,12-dimethylbenz[a]anthracene (DMBA) induced preneoplastic mammary alveolar lesions (MAL) in glands from wild-type mice and βERKO mice, but failed to induce MAL in mammary glands from αERKO mice. Microarray analysis of DMBA-treated mammary glands identified 28 functional pathways whose expression was significantly different in αERKO mice versus both βERKO and wild-type mice; key functions that were differentially expressed in αERKO mice included cell division, cell proliferation, and apoptosis. The data demonstrate distinct roles for ERα and ERβ in normal and neoplastic development in the mouse mammary gland, and suggest that EGF can mimic the ERα-mediated effects of E in this organ.

2014-10-18 | GSE62451 | GEO

Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis

Project description:Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis

| PRJNA555327 | ENA