Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

ABSTRACT: Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

PROVIDER: PRJNA1001992 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

Project description:Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

| PRJNA946021 | ENA

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

Project description:Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

| PRJNA946022 | ENA

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (scRNA-Seq)

Project description:Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (scRNA-Seq)

| PRJNA1001995 | ENA

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (Bulk RNA-Seq)

Project description:Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (Bulk RNA-Seq)

| PRJNA1001996 | ENA

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (scRNA-Seq)

Project description:Trans-differentiation from an adenocarcinoma to a small cell neuroendocrine state is associated with therapy escape in multiple cancer types. The temporal transcriptional changes of this process remain largely undefined. Here, we performed a multi-omics time course analysis of our pan-small cell neuroendocrine cancer model (termed PARCB), a forward genetic transformation using human prostate basal cells. With integrative analyses of RNA sequencing and ATAC sequencing, a shared developmental trajectory is identified among all transformed patient samples. Further mapping with single cell resolution reveals two distinct lineages defined by mutually exclusive expression of ASCL1 and ASCL2. Temporal regulation by groups of transcription factors across developmental stages reveals that cellular reprogramming precedes the induction of neuronal programs. Lastly, TFAP4 and ASCL1/2 feedback were identified as potential regulators of ASCL1 and ASCL2 expression. Our study provides temporal transcriptional patterns and uncovers pan-tissue parallels between prostate and lung cancers, and normal neuroendocrine cells.

2023-11-24 | GSE240056 | GEO

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation (Bulk RNA-Seq)

2023-11-24 | GSE240057 | GEO

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation.

Project description: Not available

| S-EPMC10878415 | biostudies-literature

Temporal evolution reveals bifurcated lineages in aggressive neuroendocrine small cell prostate cancer trans-differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-24 | GSE240058 | GEO

DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

Project description:Neuroendocrine prostate cancer (NEPC) is an aggressive, treatment-resistant subtype of prostate cancer characterized by poor prognosis and limited therapeutic options. In this study, we identify de novo DNA methyltransferase 3B (DNMT3B) as a critical driver of NEPC growth and neuroendocrine differentiation. We demonstrate that DNMT3B expression is significantly upregulated during prostate cancer progression and is essential for NEPC cell proliferation, as its genetic inhibition via CRISPR-Cas9 and inducible shRNA systems impairs tumor growth and promotes apoptosis both in vitro and in vivo. Transcriptomic profiling reveals that DNMT3B loss disrupts cell cycle regulation and suppresses neuroendocrine lineage programs by downregulating key transcription factors such as FOXA2, NEUROD1, SOX2, and INSM1. Moreover, DNMT3B is required for both the initiation and maintenance of NEPC in a human genetically engineered prostate cancer model. Pharmacological inhibition of DNMT3B with Nanaomycin A selectively suppresses NEPC tumor growth and attenuates neuroendocrine marker expression without causing systemic toxicity. These findings establish DNMT3B as a central regulator of NEPC and support its potential as a therapeutic target for this lethal cancer subtype

2026-07-30 | GSE302864 | GEO

DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

Project description:DNMT3B drives neuroendocrine lineage plasticity and aggressive progression in prostate cancer

| PRJNA1292727 | ENA