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Transcriptome analyses of luminal-derived basal cells induced by hormones in the mammary gland

ABSTRACT: Transcriptome analyses of luminal-derived basal cells induced by hormones in the mammary gland

PROVIDER: PRJNA431360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6506113_1.fastq.gz	Fastqsanger.gz
	SRR6506113_2.fastq.gz	Fastqsanger.gz
	SRR6506114_1.fastq.gz	Fastqsanger.gz
	SRR6506114_2.fastq.gz	Fastqsanger.gz
	SRR6506115_1.fastq.gz	Fastqsanger.gz

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Transcriptome analyses of luminal-derived basal cells induced by hormones in the mammary gland

Project description:We have used RNA-seq to examine RNA differential expression among three populations, normal basal cells, luminal-derived basal cells (LdBCs) and normal luminal cells.

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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

Transcriptome analysis of luminal and basal cell subpopulations in the lactating versus pregnant mammary gland

Project description:To identify genes specifically expressed in lactating mammary glands, the gene expression profiles of luminal and basal cells from different developmental stages were compared. Comparison of gene expression in luminal and basal cells harvested from the mammary glands of virgin, 18.5 day pregnant and 2 day lactating mice (2 mice per stage).

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Hormones induce the formation of luminal-derived basal cells in the mammary gland.

Project description:In the mammary gland, it is widely believed that the luminal cells are unipotent after birth, contributing only to the luminal compartment in normal development. Here, by lineage tracing, we uncovered an unexpected potential of luminal cells that can give rise to basal cells during pregnancy. These luminal-derived basal cells (LdBCs) persisted through mammary regression and generated more progeny in successive rounds of pregnancies. LdBCs express basal markers as well as estrogen receptor α (ERα). In ovariectomized (OVX) mice, stimulation with estrogen and progesterone promoted the formation of LdBCs. In serial transplantation assays, LdBCs were able to reconstitute new mammary glands in a hormone-dependent manner. Transcriptome analysis and genetic experiments suggest that Wnt/β-catenin signaling is essential for the formation and maintenance of LdBCs. Our data uncover an unexpected bi-potency of luminal cells in a physiological context. The discovery of ERα+ basal cells, which can respond to hormones and are endowed with stem cell-like regenerative capacity in parous mammary gland, provides new insights into the association of hormones and breast cancer.

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The histone demethylase KDM6A controls the mammary luminal lineage through enzyme-independent mechanisms

Project description:Mammary ducts and alveoli are composed of basal and luminal cells, with the fate and differentiation of secreting cells being controlled by hormones through specific transcription factors. This study establishes the essential role of the histone H3 lysine 27 trimethylation (H3K27me3) demethylase KDM6A (UTX) in a balanced basal and luminal cell compartment. Disproportionate formation of basal cells in the absence of KDM6A resulted in disorganized mammary ducts and alveoli and lactation failure. Mutant luminal progenitors lost their distinctive transcription factor expression pattern and acquired basal characteristics leading to a preferential expansion of this lineage. The structure of mammospheres obtained from mutant progenitors suggested they were derived from basal progenitors. The genomic H3K27me3 landscape was unaltered in the absence of KDM6A suggesting demethylase-independent mechanisms. In support of this, mammary tissue developed normally in mice expressing a catalytically inactive KDM6A. This study demonstrated that mammary luminal progenitor cells rely on UTX to stably maintain their identity and thereby establish a balance of basal and luminal cells required for a functional mammary gland.

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LPA receptor activity is basal specific and coincident with early pregnancy and involution during mammary gland postnatal development

Project description:During pregnancy, luminal and basal epithelial cells of the adult mammary gland proliferate and differentiate resulting in remodeling of the adult gland. While pathways that control this process have been characterized in the gland as a whole, the contribution of specific cell subtypes, in particular the basal compartment, remains largely unknown. Basal cells provide structural and contractile support, however they also orchestrate the communication between the stroma and the luminal compartment at all developmental stages. Using RNA-seq, we show that basal cells are extraordinarily transcriptionally dynamic throughout pregnancy when compared to luminal cells. We identified gene expression changes that define specific basal functions acquired during development that led to the identification of novel markers. Enrichment analysis of gene sets from 24 mouse models for breast cancer pinpoint to a potential new function for insulin-like growth factor 1 (Igf1r) in the basal epithelium during lactogenesis. We establish that β-catenin signaling is activated in basal cells during early pregnancy, and demonstrate that this activity is mediated by lysophosphatidic acid receptor 3 (Lpar3). These findings identify novel pathways active during functional maturation of the adult mammary gland.

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Project description:Recent studies demonstrate both basal and luminal cells of the prostate gland can initiate tumorigenesis upon oncogenic transformation. However, it remains unclear how molecular mechanisms operating within each cell lineage contribute to the initiation and progression of the prostate cancer. Here we investigate functions of individual miRNAs using genetically engineered mouse models. By both quantitative miR-Seq and in situ hybridization, we identify microRNA-205 (miR-205) as the most highly expressed miRNA and specific to the basal cells in the prostate. MicroRNA-205 expression is further elevated in the basal cells in the well-established Pten null tumorigenic mouse model. To investigate the role of miR-205 in Pten-deletion mediated tumorigenesis, we generated a Pten/miR-205 double knockout mouse model. Concurrent deletion of both miR-205 and Pten significantly compromised tumor progression in both basal and luminal compartments. We observed significantly reduced tumor size and compromised proliferation in both basal and luminal cells. We have previously demonstrated a critical requirement of miR-205 for maintaining the PI(3)K signaling and pAkt levels in skin stem cells. Consistent with this role, we observed strong reduction of pAkt and significantly increased cellular senescence in the basal cells of the dKO, compared to the Pten KO alone. These results suggest that miR-205 is cell-autonomously required for the tumorigenesis of the basal cells. Taken together, we have identified miR-205 as an important regulator in prostate cancer. Our study also reveals an essential and unexpected role of the basal cells for promoting prostate tumorigenesis.

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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

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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

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