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

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

PROVIDER: PRJNA1001996 | ENA |

REPOSITORIES: ENA

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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

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

| PRJNA1001992 | 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

| PRJNA946021 | 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 (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:This SuperSeries is composed of the SubSeries listed below.

2023-11-24 | GSE240058 | GEO

Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

Project description:Neuroendocrine prostate cancer (NEPC) is an aggressive, androgen-independent variant of prostate cancer (PCa) that most commonly develops in patients as a mechanism of therapeutic resistance. The underlying mechanisms driving PCa lineage plasticity and trans-differentiation to a neuroendocrine lineage are not fully understood. Here, we identify Notch signaling as a key suppressor of neuroendocrine differentiation in PCa. Restoration of Notch signaling in NEPC models results in phenotypic conversion towards a non-neuroendocrine state with expression of prostate luminal cell markers and immunologic changes including up-regulation of MHC Class I and II and type I interferon signaling that correlate with changes in the tumor immune microenvironment. Overall, these data provide new insights into how Notch signaling influences PCa lineage plasticity and points to new therapeutic avenues to modulate it.

2024-08-28 | GSE234819 | GEO

Notch signaling suppresses neuroendocrine differentiation and alters the tumor immune microenvironment in advanced prostate cancer

2024-08-01 | GSE235036 | GEO

Siah2-dependent concerted activity of HIF and FoxA2 regulates formation of neuroendocrine prostate tumors

Project description:Neuroendocrine (NE) carcinoma and NE differentiation (NED) of human prostate tumor are hallmarks of aggressive human prostate cancer. Here we reveal that HIF-1a cooperation with FoxA2, a transcription factor expressed in NE tissue, is required for determining NE phenotype. Reduced HIF-1a expression, as seen in the E3 ubiquitin ligase Siah2 mutant mice, converted NE tumors to atypical hyperplasia when crossed with the TRAMPTg mice. Significantly, HIF-1a cooperation with FoxA2 enables the trans-activation of select HRE-regulated genes such as Hes6, Plod2 and Jmjd1a, whose expression is notably higher in metastatic prostate adenocarcinomas. Our findings disclose the requirement for spatial and timely regulation of FoxA2 and HIF-1a for NE/NED in prostate tumors. 12 prostate tumor samples were analyzed during normoxia and hypoxia, with different FOX/HIF genotypes. The pivotal samples are represented as duplicates.

2010-07-13 | E-GEOD-18478 | biostudies-arrayexpress

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