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ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scRNA-seq]

ABSTRACT: ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scRNA-seq]

PROVIDER: PRJNA1080200 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28085772_1.fastq.gz	Fastqsanger.gz
	SRR28085772_2.fastq.gz	Fastqsanger.gz
	SRR28085773_1.fastq.gz	Fastqsanger.gz
	SRR28085773_2.fastq.gz	Fastqsanger.gz
	SRR28085774_1.fastq.gz	Fastqsanger.gz

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ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scRNA-seq]

Project description:Performed scRNA-seq of an autochthonous mouse model at an early stage of disease initiation. Despite broad expression of ERG in all prostate epithelial cells, proliferation was enriched in a small, stem-like population of cells with mixed-luminal basal identity (intermediate cells).

2025-04-07 | GSE257543 | GEO

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ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scATAC-seq]

Project description:ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scATAC-seq]

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ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity [scATAC-seq]

Project description:Performed scATAC-seq in 3 timepoints of an autochthonous mouse model. A proliferative population is characterized by an ERG-specific chromatin state enriched for NFkB, AP-1, STAT and NFAT binding, with implications for TF cooperativity. ERG is enriched in a small stem-like population implicates the chromatin context of these cells as a critical variable for unmasking its oncogenic activity.

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ERG activates a stem-like proliferation-differentiation program in prostate epithelial cells with mixed basal-luminal identity.

Project description:To gain insight into how ERG translocations cause prostate cancer, we performed single cell transcriptional profiling of an autochthonous mouse model at an early stage of disease initiation. Despite broad expression of ERG in all prostate epithelial cells, proliferation was enriched in a small, stem-like population with mixed-luminal basal identity (called intermediate cells). Through a series of lineage tracing and primary prostate tissue transplantation experiments, we find that tumor initiating activity resides in a subpopulation of basal cells that co-express the luminal genes Tmprss2 and Nkx3.1 (called BasalLum) but not in the larger population of classical Krt8+ luminal cells. Upon ERG activation, BasalLum cells give rise to the highly proliferative intermediate state, which subsequently transitions to the larger population of Krt8+ luminal cells characteristic of ERG-positive human cancers. Furthermore, this proliferative population is characterized by an ERG-specific chromatin state enriched for NFkB, AP-1, STAT and NFAT binding, with implications for TF cooperativity. The fact that the proliferative potential of ERG is enriched in a small stem-like population implicates the chromatin context of these cells as a critical variable for unmasking its oncogenic activity.

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ERG-driven gene expression in basal and luminal cells of mouse prostate organoids

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Lineage plasticity enables low-ER luminal tumors to evolve and gain basal-like traits

Project description:Breast tumors expressing lower levels of Estrogen Receptor (ER) represent a distinct subset of breast cancer characterized by the emergence of basal-like characteristics within tumors that are traditionally considered luminal-like. Lineage tracing of these low-ER tumors in the MMTV-PyMT mouse mammary tumor model revealed that the basal-like tumor cells within these tumors arose from normal luminal epithelial cells, suggesting that luminal-to-basal plasticity is responsible for the evolution and emergence of basal-like characteristics within these tumors. This study aims to identify the potential drivers of this plasticity by using single-cell RNA sequencing to identify populations of lineage-restricted luminal cells and luminal-derived basal cells within the tumor, and comparing their gene expression profiles.

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