Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Defined cellular reprogramming of androgen receptor-active prostate cancer to neuroendocrine prostate cancer [scATAC-seq]

ABSTRACT: Defined cellular reprogramming of androgen receptor-active prostate cancer to neuroendocrine prostate cancer [scATAC-seq]

PROVIDER: PRJNA934589 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23401753_1.fastq.gz	Fastqsanger.gz
	SRR23401753_2.fastq.gz	Fastqsanger.gz
	SRR23401754_1.fastq.gz	Fastqsanger.gz
	SRR23401754_2.fastq.gz	Fastqsanger.gz
	SRR23401755_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Subtype Heterogeneity and Epigenetic Convergence in Neuroendocrine Prostate Cancer [scATAC-seq]

Project description:We analyzed chromatin accessibility, scATAC-seq and RNA-seq across neuroendocrine carcinomas from distinct anatomic origins including Merkel cell carcinomas, neuroendocrine prostate cancer, small cell lung cancer and gastrointestinal NECs.

2024-03-27 | GSE262623 | GEO

Defined cellular reprogramming of androgen receptor-active prostate cancer to neuroendocrine prostate cancer [scATAC-seq]

Project description:Neuroendocrine prostate cancer (NEPC) arises primarily through neuroendocrine transdifferentiation (NEtD) as an adaptive mechanism of therapeutic resistance. Models to define the functional effects of putative drivers of this process on androgen receptor (AR) signaling and NE cancer lineage programs are lacking. We adapted a genetically defined strategy from the field of cellular reprogramming to directly convert AR-active prostate cancer (ARPC) to AR-independent NEPC using candidate factors. We delineated critical roles of the pioneer factors ASCL1 and NeuroD1 in NEtD and uncovered their abilities to silence AR expression and signaling by remodeling chromatin at the somatically acquired AR enhancer and global AR binding sites with enhancer activity. We also elucidated the dynamic temporal changes in the transcriptomic and epigenomic landscapes of cells undergoing acute lineage conversion from ARPC to NEPC which should inform future therapeutic development. Further, we distinguished the activities of ASCL1 and NeuroD1 from the inactivation of RE-1 silencing transcription factor (REST), a master suppressor of a major neuronal gene program, in establishing a NEPC lineage state and in modulating the expression of genes associated with major histocompatibility complex class I (MHC I) antigen processing and presentation.

2024-02-09 | GSE225022 | GEO