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ATF3-induced mammary tumors exhibit molecular features of human basal-like breast cancer

ABSTRACT: ATF3-induced mammary tumors exhibit molecular features of human basal-like breast cancer

PROVIDER: PRJNA683050 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13208994_1.fastq.gz	Fastqsanger.gz
	SRR13208994_2.fastq.gz	Fastqsanger.gz
	SRR13208995_1.fastq.gz	Fastqsanger.gz
	SRR13208995_2.fastq.gz	Fastqsanger.gz
	SRR13208996_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

ATF3-induced mammary tumors exhibit molecular features of human basal-like breast cancer

Project description:Transcriptional profiling of mammary tumors that occurs in parous, BK5.ATF3 mice, compared to adjacent normal mammary tissue

2021-03-23 | GSE162804 | GEO

ATF3-Induced Mammary Tumors Exhibit Molecular Features of Human Basal-Like Breast Cancer.

Project description:Basal-like breast cancer (BLBC) is an aggressive and deadly subtype of human breast cancer that is highly metastatic, displays stem-cell like features, and has limited treatment options. Therefore, developing and characterizing preclinical mouse models with tumors that resemble BLBC is important for human therapeutic development. ATF3 is a potent oncogene that is aberrantly expressed in most human breast cancers. In the BK5.ATF3 mouse model, overexpression of ATF3 in the basal epithelial cells of the mammary gland produces tumors that are characterized by activation of the Wnt/β-catenin signaling pathway. Here, we used RNA-Seq and microRNA (miRNA) microarrays to better define the molecular features of BK5.ATF3-derived mammary tumors. These analyses showed that these tumors share many characteristics of human BLBC including reduced expression of Rb1, Esr1, and Pgr and increased expression of Erbb2, Egfr, and the genes encoding keratins 5, 6, and 17. An analysis of miRNA expression revealed reduced levels of Mir145 and Mir143, leading to the upregulation of their target genes including both the pluripotency factors Klf4 and Sox2 as well as the cancer stem-cell-related gene Kras. Finally, we show through knock-down experiments that ATF3 may directly modulate MIR145/143 expression. Taken together, our results indicate that the ATF3 mouse mammary tumor model could provide a powerful model to define the molecular mechanisms leading to BLBC, identify the factors that contribute to its aggressiveness, and, ultimately, discover specific genes and gene networks for therapeutic targeting.

| S-EPMC7956570 | biostudies-literature

BK5.ATF3-induced mammary tumors compared to normal mammary glands

Project description:Transcriptional profiling of mammary tumors that occur in parous, BK5.ATF3 mice, compared to normal mammary tissue

2021-03-23 | GSE162793 | GEO

BK5.ATF3-induced mammary tumors compared to normal mammary glands

Project description:BK5.ATF3-induced mammary tumors compared to normal mammary glands

| PRJNA683036 | ENA

Rb deletion in mammary stem/progenitor epithelium induces tumors with features of luminal-B or basal-like breast cancer

Project description:The retinoblastoma tumor suppressor, Rb, is implicated in luminal-B and basal-like breast carcinomas, yet its effect on mammary gland development and causal role in breast cancer subtypes remain undefined. Here we show that conditional deletion of Rb in mouse mammary epithelium led to expansion of the stem/progenitor cells and to focal acinar hyperplasia with squamous metaplasia. These uniform lesions progressed into histologically diverse, transplantable mammary adenocarcinomas and adenosquamous carcinomas with features of luminal-B or basal-like carcinomas. A subset of basal-like but none of the luminal-B tumors expressed mutant p53. These results demonstrate a causative role for Rb in the etiology of breast cancer subtypes and implicate p53 status as a determinant of tumor phenotype after Rb loss. Keywords: reference x sample Will be updated soon

2010-07-06 | E-GEOD-14457 | biostudies-arrayexpress

Rb deletion in mammary stem/progenitor epithelium induces tumors with features of luminal-B or basal-like breast cancer

2010-07-07 | GSE14457 | GEO

The effect of macrophage depletion on mammary basal cells

Project description:To investigate the effect of macrophages on mammary basal cells, we established a macrophage depletion mouse model by clodronate liposome (CL) intraperitoneal injection, and the mammary basal cells were collected by FACS sorting. We then performed RNA-seq analysis on clodronate liposome (CL) treated mammary basal cells compared to control.

2023-04-20 | GSE210268 | GEO

ATF3 is a central regulator of interferon-beta and interferon-stimulated genes during the innate immune response

Project description:This study shows that in the absence of Atf3, primary mouse macrophages display significantly greater basal and PRR-inducible IFNβ expression. This regulation appears to be directly on the level of Ifnb1 transcription mediated by ATF3 binding proximal to the Ifnb1 promoter under basal condition. The ATF3 expression was demonstrated to be type I IFN-inducible in both human and mouse immune cells. A subset of 36 genes downstream of IFNAR signalling were modulated in an ATF3-dependent manner.The regulation of IFN responses by ATF3 had significant relevance on in vitro viral infection. Together these findings demonstrate that ATF3 is an important regulatory handbrake that limits the magnitude of IFN responses on multiple levels; basal Ifnb1 expression; PRR-inducible IFNβ; and the expression of specific ISGs. 12 samples

2015-09-07 | E-GEOD-61055 | biostudies-arrayexpress

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.

2022-09-26 | GSE196555 | GEO

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

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