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A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer

ABSTRACT: A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer

PROVIDER: PRJNA1075686 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27947604.fastq.gz	Fastqsanger.gz
	SRR27947605.fastq.gz	Fastqsanger.gz
	SRR27947606.fastq.gz	Fastqsanger.gz
	SRR27947607.fastq.gz	Fastqsanger.gz
	SRR27947608.fastq.gz	Fastqsanger.gz

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A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (shRNA)

Project description:Neuroendocrine prostate cancer (NEPC) presents a formidable clinical challenge owing to its aggressive progression and resistance to conventional therapies. A key driver of NEPC is the overexpression of MYCN, a well-established oncogene associated with neuroendocrine tumors. However, efforts to directly inhibit the N-Myc protein encoded by this gene have resulted in limited success, thereby hindering therapeutic advancements. To overcome this obstacle, we conducted unbiased genome-wide screening using isogenic prostate cancer cell lines to identify the synthetic vulnerabilities of MYCN. Among the identified candidates, NEUROG2 emerged as a significant candidate. Neurog2 is a proneural transcription factor (PTF) known for its role in developmental processes and trans-differentiation of adult cells. Our findings demonstrate that Neurog2 depletion does not affect non-malignant cells but significantly suppresses the growth of MYCN-overexpressing cells and tumors in orthotopic NEPC models. Furthermore, our observations indicate that Neurog2-driven modulation of PTFs potentially contribute to NEPC development. Thus, targeting Neurog2 holds promise as an effective therapeutic strategy for MYCN-overexpressing NEPC.

2025-04-29 | GSE255592 | GEO

A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (CRISPR)

2025-04-29 | GSE255591 | GEO

A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (shRNA)

Project description:A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (shRNA)

| PRJNA1075691 | ENA

A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (CRISPR)

Project description:A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer (CRISPR)

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Expression profiling of murine MYCN-driven neuroendocrine tumor from LSL-MYCN;hGFAP-Cre mice.

Project description:MYCN overexpression is a hallmark of many tumors originating from neural cell precursors. We generated a transgenic mouse with Cre-conditional induction of MYCN in glial fibre acidic protein (GFAP) expressing cells resulting in the development of neuroendocrine tumors of the pancreas and the brain. The expression profiles of nine tumors from pancreas and three brain tumors were compared to non-malignant pancreas controls (GSM771025.CEL-GSM771027.CEL) from wildtype mice Expression profiles of tumors and controls were analysed using GSEA and ANOVA.

2016-03-01 | E-GEOD-73466 | biostudies-arrayexpress

Expression profiling of murine MYCN-driven neuroendocrine tumor from LSL-MYCN;hGFAP-Cre mice.

2016-03-01 | GSE73466 | GEO

A novel role for Neurog2 in MYCN driven neuroendocrine plasticity of prostate cancer

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

2025-04-29 | GSE255593 | GEO

Recruitment of BRCA1 limits MYCN-driven accumulation of stalled RNA Polymerase in neuroblastoma

Project description:Deregulation of the MYCN gene drives the development of neuronal and neuroendocrine tumors and is often associated with a particularly poor prognosis. Here we show that activation of MYCN in human neuroblastoma cells induces promoter escape of RNAPII. If pause release of RNAPII fails, MYCN recruits the BRCA1 protein to promoter-proximal regions. Recruitment of BRCA1 prevents MYCN-dependent accumulation of stalled RNAPII and enhances transcriptional activation by MYCN. Mechanistically, BRCA1 stabilizes mRNA de-capping complexes and enables MYCN to suppress R-loop formation in promoter-proximal regions. Recruitment of BRCA1 is mediated by the ubiquitin-specific protease, USP11, which binds specifically to MYCN that is de-phosphorylated at Thr58. Thr58 phosphorylation promotes proteasomal turnover of MYCN, hence BRCA1 stabilizes chromatin association of MYCN. Since BRCA1 is highly expressed in neuronal progenitor cells during early development and since MYC is less efficient than MYCN in recruiting BRCA1, our findings argue that a cell lineage-specific stress response enables MYCN-driven tumors to cope with deregulated RNAPII function.

2019-03-21 | GSE111905 | GEO

Gene expression profiling of MYCN-driven neuroblastoma tumor development in the TH-MYCN mouse model.

Project description:Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system progenitor cells. MYCN and ALK are driver oncogenes both of which are specifically expressed during early neurogenesis. This is in line with the assumption that neuroblastoma arises through disruption of normal developmental processes. MYCN has a broad impact on the tumor phenotype; however, the details of the MYCN driven oncogenic program are far from clear. In order to gain further insight into the role of gene expression during neuroblastoma initiation and progression, we evaluated gene expression profiles of hyperplastic ganglia and tumors isolated from MYCN transgenic mice.

2016-02-28 | E-MTAB-3247 | biostudies-arrayexpress

Metabolic dependencies in MYCN-driven neuroblastoma

Project description:Here we sought metabolic alterations specifically associated with amplified MYCN as nodes to indirectly target the MYCN oncogene. Liquid chromatography-mass spectrometry-based proteomics identified 7 proteins consistently correlated with MYCN in proteomes from 49 neuroblastoma biopsies and 13 cell lines. Among these were phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme in de novo serine synthesis. MYCN associated with two regions in the PHGDH promoter, supporting transcriptional PHGDH regulation by MYCN. Pulsed stable isotope-resolved metabolomics utilizing 13C-glucose labeling demonstrated higher de novo serine synthesis in MYCN-amplified cells compared to cells with diploid MYCN. An independence of MYCN-amplified cells from exogenous serine and glycine was demonstrated by serine and glycine starvation, which attenuated nucleotide pools and proliferation only in cells with diploid MYCN but did not diminish these endpoints in MYCN-amplified cells. Proliferation was attenuated in MYCN-amplified cells by CRISPR/Cas9-mediated PHGDH knockout or treatment with PHGDH small molecule inhibitors without affecting cell viability. PHGDH inhibitors administered as single-agent therapy to NMRI-Foxn1nu/nu mice harboring patient-derived MYCN-amplified neuroblastoma xenografts slowed tumor growth. However, combining a PHGDH inhibitor with the standard-of-care chemotherapy drug, cisplatin, revealed antagonism of chemotherapy efficacy in vivo. Emergence of chemotherapy resistance was confirmed in the genetic PHGDH knockout model in vitro. Altogether, PHDGH knockout and inhibition by small molecules consistently slows proliferation, but stops short of killing the cells, which then establish resistance to classical chemotherapy. Although PHGDH inhibition with small molecules has produced encouraging results in other preclinical cancer models, this approach must be considered with caution in patients with neuroblastoma.

2020-12-11 | PXD018300 | Pride

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