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Schwann cell plasticity regulates neuroblastic tumor cell differentiation

ABSTRACT: Schwann cell plasticity regulates neuroblastic tumor cell differentiation

PROVIDER: PRJNA615860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11434500.fastq.gz	Fastqsanger.gz
	SRR11434501.fastq.gz	Fastqsanger.gz
	SRR11434502.fastq.gz	Fastqsanger.gz
	SRR11434503.fastq.gz	Fastqsanger.gz
	SRR11434504.fastq.gz	Fastqsanger.gz

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Schwann cell plasticity regulates neuroblastic tumor cell differentiation

Project description:The remarkable plasticity of Schwann cells (SCs) is essential for nerve regeneration but also contributes to neuropathies and cancer progression. It has not yet been investigated whether the adaptive potential of SCs is manifested in stromal, tumor associated SCs characteristically found within a benign subtype of neuroblastic tumors (NBTs). We here performed transcriptome profiling of human NBTs, rich and poor in SC stroma, as well as human injured nerves, rich in repair SCs, revealing that stromal SCs exhibit a repair SC characteristic gene expression signature. In turn, primary repair SCs had a pro-differentiating and anti-proliferative effect on NBT cell lines after direct and trans-well co-culture. Within the pool of secreted stromal/repair SC factors, we identified EGFL8, a matricellular protein with so far undescribed function, to induce neuronal differentiation of aggressive NBT cells. EGFL8 expression further correlated with favorable tumor stage and increased patient survival. Our findings suggest that stromal SCs exert nerve repair associated functions in the tumor-environment and underline the therapeutic value of SC-derived factors for aggressive, SC stroma-poor NBTs.

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Malignant Schwann cell precursors mediate intratumoral plasticity in human neuroblastoma

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Project description:Peripheral glial Schwann cells switch to a repair state after nerve injury, proliferate to supply lost cell population, migrate to form regeneration tracks, and generates a permissive microenvironment for nerve regeneration. Exploring essential regulators of the repair responses of Schwann cells may benefit the clinical treatment for peripheral nerve injury. In the present study, FOSL1 regulates Schwann cell phenotype modulation and provided a novel therapeutic approach to orchestrate the regeneration and functional recovery of injured peripheral nerves.

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Vitamin C regulates Schwann cell myelination by promoting DNA demethylation of pro-myelinating genes

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Schwann cell plasticity regulates neuroblastic tumor cell differentiation via epidermal growth factor-like protein 8.

Project description:Adult Schwann cells (SCs) possess an inherent plastic potential. This plasticity allows SCs to acquire repair-specific functions essential for peripheral nerve regeneration. Here, we investigate whether stromal SCs in benign-behaving peripheral neuroblastic tumors adopt a similar cellular state. We profile ganglioneuromas and neuroblastomas, rich and poor in SC stroma, respectively, and peripheral nerves after injury, rich in repair SCs. Indeed, stromal SCs in ganglioneuromas and repair SCs share the expression of nerve repair-associated genes. Neuroblastoma cells, derived from aggressive tumors, respond to primary repair-related SCs and their secretome with increased neuronal differentiation and reduced proliferation. Within the pool of secreted stromal and repair SC factors, we identify EGFL8, a matricellular protein with so far undescribed function, to act as neuritogen and to rewire cellular signaling by activating kinases involved in neurogenesis. In summary, we report that human SCs undergo a similar adaptive response in two patho-physiologically distinct situations, peripheral nerve injury and tumor development.

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Project description:Androgen receptor cell-autonomously regulates luminal cell plasticity [ATAC-Seq]

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