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

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

PROVIDER: PRJNA764741 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15980100_1.fastq.gz	Fastqsanger.gz
	SRR15980100_2.fastq.gz	Fastqsanger.gz
	SRR15980101_1.fastq.gz	Fastqsanger.gz
	SRR15980101_2.fastq.gz	Fastqsanger.gz
	SRR15980102_1.fastq.gz	Fastqsanger.gz

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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

Microarray expression profiling study of Runx1-null and wild type luminal mammary epithelial cells

Project description:RUNX1 encodes a RUNX family transcription factor (TF) and was recently identified as a novel mutated gene in human luminal breast cancers. We found that Runx1 is expressed in all subpopulations of murine mammary epithelial cells (MECs) except the secretory alveolar luminal cells. Conditional knockout of Runx1 in MECs by MMTV-Cre led to a decrease in luminal MECs, largely due to a profound reduction in the estrogen receptor (ER)-positive mature luminal subpopulation, a phenotype that could be rescued by loss of either Trp53 or Rb1. Mechanistically RUNX1 represses Elf5, a master regulatory TF gene for alveolar cells, and activates Foxa1, a key mature luminal TF gene involved in the ER program. Collectively, our data identified a key regulator of the ER+ luminal lineage whose disruption may contribute to development of ER+ luminal breast cancer when under the background of either TP53 or RB1 loss. Thoracic and inguinal mammary glands from 3 MMTV-Cre;Runx1L/L;R26Y and 3 MMTV-Cre;Runx1+/+;R26Y adult virgin females were dissected out, minced and digested to single cell suspension. Runx1L is the floxed conditional knockout allele of Runx1. R26Y is a conditional YFP reporter that would be turned on upon Cre-mediated recombination. FACSaria machine was used to sort out the YFP-marked luminal epithelial cell population of each of these 6 mice. Total RNA was isolated with Qiagen RNeasy kit and subsequently amplified by Nugen V2 and applied to Affymetrix mouse genome 430 2.0 arrays.

2014-11-26 | E-GEOD-47375 | biostudies-arrayexpress

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Project description:CD19 + ER1 (B lymphocyte line) cells differentiated into CD45 + Ter119 + ter cells in vitro, we selected CD19 + ER1 cells (CD19+CD45+TER119-CD11b+), intermediate ER1 cells (CD19-CD45+TER119-CD11b+) and Ter119 + CD45 + CD19 - ER1 cells (CD19-CD45+TER119+CD11b+) for transcriptome analysis. We then performed gene expression profiling analysis using data obtained from RNA-seq of those 3 cell lines.

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Microarray expression profiling study of Runx1-null and wild type luminal mammary epithelial cells

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Curtobacterium sp. ER1/6

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Runx1 marks a luminal castration resistant lineage established at the onset of prostate development

Project description:Runx1 marks a luminal castration resistant lineage established at the onset of prostate development

| PRJNA637837 | ENA

Runx1 marks a luminal castration resistant lineage established at the onset of prostate development

Project description:We performed scRNA-seq to characterize the heterogeneity of RUNX1+ and RUNX1- fractions of the adult mouse prostate. We dissected individual lobes of intact/hormone naive and regressed/castrated mouse prostates, isolated from P2-Runx1:RFP reporter mice, expressing RFP as a surrogate of Runx1 expression. In order to compensate for the relative sparsity of RFP+ and RFP- cells respectively pre- and post-castration, we artificially enriched for under-represented populations by FACS (EPCAM+) prior cell encapsulation. To study the specification of embryonic prostate lineages, we performed scRNA-seq on the EPCAM+ fraction of UGS explant cultures collected at successive time points: E15.5 (D0), day 1 (D1), day 3 (D3), and day 6 (D6).

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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

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