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Embryonic neural crest cell derivatives release pro-metastatic cues driving neuroblastoma dissemination in an avian disease model

ABSTRACT: Embryonic neural crest cell derivatives release pro-metastatic cues driving neuroblastoma dissemination in an avian disease model

PROVIDER: PRJNA716104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14026419.fastq.gz	Fastqsanger.gz
	SRR14026420.fastq.gz	Fastqsanger.gz
	SRR14026421.fastq.gz	Fastqsanger.gz
	SRR14026422.fastq.gz	Fastqsanger.gz
	SRR14026423.fastq.gz	Fastqsanger.gz

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Embryonic neural crest cell derivatives release pro-metastatic cues driving neuroblastoma dissemination in an avian disease model

Project description:Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. Neuroblastoma (NB) is an emblematic example, arising from neural crest progenitors and characterized by a high heterogeneity and a widely disseminated clinical presentation. Metastatic triggers from the embryonic environment are suspected but yet unknown due to limited investigation access in patients and current models. Using combinations of ex vivo and in vivo models mimicking the embryonic context coupled to proteomic and transcriptomic analyses, we identify Olfactomedin1 (OLFM1) released by sympathetic derivatives at the core of a gene program promoting NB cells decohesion, primary tumor escape and dissemination. This OLFM signature discriminates metastatic from localized stages in NB patient cohorts. Finally, we report an extended tumor cell escape gene signature of disseminated forms specifically shared by cancers with neural-crest origin, revealing a sustained embryonic imprint of the lineage of origin, manifested in the metastatic properties of malignant cells.

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Environmental cues from neural crest derivatives act as metastatic triggers in an embryonic neuroblastoma model.

Project description:Embryonic malignant transformation is concomitant to organogenesis, often affecting multipotent and migratory progenitors. While lineage relationships between malignant cells and their physiological counterparts are extensively investigated, the contribution of exogenous embryonic signals is not fully known. Neuroblastoma (NB) is a childhood malignancy of the peripheral nervous system arising from the embryonic trunk neural crest (NC) and characterized by heterogeneous and interconvertible tumor cell identities. Here, using experimental models mimicking the embryonic context coupled to proteomic and transcriptomic analyses, we show that signals released by embryonic sympathetic ganglia, including Olfactomedin-1, induce NB cells to shift from a noradrenergic to mesenchymal identity, and to activate a gene program promoting NB metastatic onset and dissemination. From this gene program, we extract a core signature specifically shared by metastatic cancers with NC origin. This reveals non-cell autonomous embryonic contributions regulating the plasticity of NB identities and setting pro-dissemination gene programs common to NC-derived cancers.

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