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GATA-3 maintains luminal cell differentiation in the mammary gland and in breast cancer

ABSTRACT: We have identified GATA-3 as a critical regulator of luminal cell differentiation in the mammary gland. Acute loss of GATA-3 in the adult mammary gland leads to an expansion of an undifferentiated luminal epithelium and the formation of a multi-layered epithelium. Here we report microarray analysis of mammary glands that have undergone acute loss of GATA-3 Keywords: genetic modification

ORGANISM(S): Mus musculus

PROVIDER: GSE5602 | GEO | 2006/10/24

SECONDARY ACCESSION(S): PRJNA96887

REPOSITORIES: GEO

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GATA-3 maintains luminal cell differentiation in the mammary gland and in breast cancer

Project description:We have identified GATA-3 as a critical regulator of luminal cell differentiation in the mammary gland. Acute loss of GATA-3 in the adult mammary gland leads to an expansion of an undifferentiated luminal epithelium and the formation of a multi-layered epithelium. Here we report microarray analysis of mammary glands that have undergone acute loss of GATA-3 Adult GATA-3flox/flox; WAP-rtTA-Cre and GATA-flox/+; WAP-rtTA-Cre mice were administered doxyxcline for 5 days and their mammary glands harvested. Total RNA was extracted by the Trizol method. Het mammary gland total RNA was labeled with Cy5 while Null mammary gland total RNA was labeled with Cy3. Microarray hybridization was performed on spotted oligonucleotide microarrays with 38,000 features. Lowess print-tip normalization and analysis was performed on the Acuity software package (V 4.0)

2010-07-01 | E-GEOD-5602 | biostudies-arrayexpress

Transcription profiling of mouse normal mammary gland epithelial populations: basal/myoepithelial, luminal estrogen receptor negative (ER-) and luminal estrogen receptor positive (ER+) cells

Project description:The goal of the experiment was to carry out a transcriptome analysis of the three main epithelial cell populations of the mouse mammary gland, the basal/myoepithelial, luminal estrogen receptor negative (ER-) and luminal estrogen receptor positive (ER+) cells, to identify cell-type specific differences in gene expression. Three replicates arrays were carried out for each of the three populations (a total of nine arrays). Each replicate was a genuine biological replicate from RNA harvested from completely independent cell preparations. Each sample was isolated from preparations of mammary epithelium derived fourth mammary fat pads of 8 * 10 week old virgin female FVB mice. Each preparation was from a pool of 10 * 20 animals (20 * 40 fat pads).

2009-04-20 | E-TABM-683 | biostudies-arrayexpress

Proteomic and phosphoproteomic profiling of human myoepithelial and luminal epithelial cells

Project description:The aim of the project is to perform deep proteomic and phosphoproteomic profiling of luminal epithelial and myoepithelial cells from the mammary gland of young vs. older women.

2022-02-16 | PXD022691 | Pride

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

A Runx1-enhancer element eR1 identified lineage restricted mammary luminal stem cells

Project description:Mammary gland homeostasis is maintained by adult tissue stem-progenitor cells residing within the luminal and basal epithelia. Dysregulation of mammary stem cells is a key mechanism for cancer development. However, stem cell characterization is challenging because reporter models using cell-specific promoters do not fully recapitulate the mammary stem cell populations. We previously found that a 270-basepair Runx1 enhancer element, named eR1, marked stem cells in the blood and stomach. Here, we identified eR1 activity in a rare subpopulation of the ERα-negative luminal epithelium in mouse mammary glands. Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli – eR1 therefore specifically marks lineage-restricted luminal stem cells. eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERα expression. Our findings demonstrate a definitive role for Runx1 in the regulation of the eR1-positive luminal stem cell proliferation during mammary homeostasis. Our findings identify a mechanistic link for Runx1 in stem cell proliferation and its dysregulation in breast cancer. Runx1 inactivation is therefore likely to be an early hit in the cell-of-origin of ERα+ luminal type breast cancer.

2021-09-22 | GSE184481 | GEO

Laminin-binding integrins are essential for the maintenance of functional secretory epithelium in lactation [luminal cells]

Project description:Integrin dimers α3/β1, α6/β1 and α6/β4 are the mammary epithelial cell receptors for laminins, which are major components of the basement membrane, a specialized extracellular matrix surrounding the mammary epithelium. The roles of specific basement membrane components and their integrin receptors in the regulation of functional gland development have not been analyzed in detail. To investigate the functions of laminin-binding integrins, we obtained mutant mice with mammary luminal cell-specific deficiencies of the α3 and α6 integrin chains generated by the Cre-Lox approach. During pregnancy, mutant mice displayed low levels of luminal progenitor activity and retarded lobulo-alveolar development, whereas their mammary glands seemed to be functional at the onset of lactation. Myoepithelial cell morphology was markedly altered in mutant glands, suggesting cellular compensation mechanisms involving cytoskeleton reorganization. However, lactation was not sustained in mutant mice, and the glands underwent precocious involution. Inactivation of the p53 gene rescued the growth defects but did not restore lactogenesis in mutant mice. This study reveals an essential role for laminin-binding integrins in functional mammary gland development.

2020-02-04 | GSE132349 | GEO

Regulation of mammary luminal cell differentiation and tumorigenesis by p38α

Project description:Mammary stem and progenitor cells are essential for mammary gland homeostasis and are also candidates for cells of origin of mammary tumors. Here, we provide evidence that the protein kinase p38a is required for the differentiation of luminal progenitor cells through modulation of the transcription factors Runx1 and Foxa1. Moreover, using a mouse model for breast cancer initiated by luminal cells, we show that p38a downregulation in mammary epithelial cells reduces tumorigenesis, which correlates with reduced numbers of tumor-initiating cells. Our results identify p38a as a key regulator of luminal progenitor cell fate that facilitates mammary tumor formation.

2017-12-28 | GSE92877 | GEO

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

2010-07-07 | GSE14457 | GEO

Expression profiling of MMTV-PyMT tumors retrovirally over-expressing GATA-3

Project description:The primary cause of mortality in breast cancer is metastasis, a process which is still poorly understood. To study the process of breast cancer metastasis, we isolated focal hyperplasias from the MMTV-PyMT transgenic breast cancer model and transplanted to syngeneic hosts. The transplants underwent stereotyped progression to adenoma, early carcinoma, and late carcinoma at 5, 8 and 18 weeks post-transplant, respectively. We compared the gene expression profiles of adenomas and late carcinomas by microarray. Analysis of the data revealed that the most differentially expressed gene family between adenomas and late carcinomas were luminal differentiation genes, among them GATA-3. Adenomas were uniformly immunopositive for GATA-3, whereas early carcinomas displayed partial loss of GATA-3. Disseminated tumour cells and 18-week late carcinomas were invariably GATA-3 negative. We found that re-introduction of GATA-3 in late carcinomas induced markers of luminal differentiation and inhibited tumour dissemination to distant sites. Keywords: spotted oligonucleotide Full length GATA-3 was cloned into the PMIG retroviral vector, which contains an IRES-GFP cassette. Primary cultures of non-fluorescent MMTV-PyMT carcinomas were infected with the GATA-3 and control retroviruses and transplanted back into the cleared mammary fat pads of wild-type mice. After six weeks of growths, tumors were isolated and total RNA harvested by the Trizol method. Total RNA from GATA-3 infected tumor outgrowths were compared to empty vector infected tumor outgrowths.

2010-07-01 | E-GEOD-5223 | biostudies-arrayexpress

Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A

Project description:Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B that mediate cytokine signaling. To reveal the underlying causes for this developmental block we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and their ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally-controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Taken together, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells. The mammary tissues from two mice of each genotype were collected 6 days (sample 9 and 11 were WT)

2009-10-21 | E-GEOD-17723 | biostudies-arrayexpress

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