Search bioRxiv⌕ Search

bioRxiv · 10.1101/2020.04.01.019422

Schwann cell plasticity regulates neuroblastic tumor cell differentiation

Abstract

The remarkable plasticity of Schwann cells (SCs) enables the acquisition of repair-specific functions essential for peripheral nerve regeneration. We hypothesized that this plastic potential is manifested in stromal SCs found within mostly benign-behaving peripheral neuroblastic tumors. To shed light on the cellular state and impact of stromal SCs, we combined transcriptome and proteome profiling of human ganglioneuromas and neuroblastomas, rich and poor in SC-stroma, respectively, as well as human injured nerve explants, rich in repair SCs. The results revealed a nerve repair-characteristic gene expression signature of stromal SCs. In turn, primary repair SCs had a pro-differentiating and anti-proliferative effect on aggressive neuroblastoma 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 neuroblastoma cell lines. This study indicates that human SCs undergo a similar adaptive response in two patho-physiologically distinct situations, peripheral nerve injury and tumor development. This response is mediated by EGFL8 and other SC derived factors, which might be of therapeutic value for neuroblastic tumors and nerve regeneration. SYNOPSIS O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=156 SRC="FIGDIR/small/019422v2_ufig1.gif" ALT="Figure 1"> View larger version (33K): org.highwire.dtl.DTLVardef@14cb89forg.highwire.dtl.DTLVardef@1ecd06aorg.highwire.dtl.DTLVardef@66f08corg.highwire.dtl.DTLVardef@3a9962_HPS_FORMAT_FIGEXP M_FIG C_FIG In order to investigate the nature of stromal Schwann cells in benign peripheral neuroblastic tumors (ganglioneuromas), we compared the cellular state of stromal Schwann cells with repair-associated Schwann cells emerging in peripheral nerves after injury. O_LIStromal Schwann cells in ganglioneuromas and repair Schwann cells in injured nerves share the expression of nerve repair-associated genes. C_LIO_LINeuroblastoma cell lines, derived from high-risk metastatic peripheral neuroblastic tumors (neuroblastomas), respond to primary repair Schwann cells and their secretome with increased neuronal differentiation and reduced proliferation. C_LIO_LIStromal and repair Schwann cells express the matricellular protein EGFL8, which is capable to induce neuronal differentiation of neuroblastoma cell lines in recombinant form. C_LI THE PAPER EXPLAINEDO_ST_ABSProblemC_ST_ABSIn response to peripheral nerve damage, Schwann cells (SCs) are able to transform into specialized repair cells essential for nerve cell regeneration. Our previous studies indicated that this reactive/adaptive potential of human SCs is not restricted to injured nerve cells but also emerges in response to peripheral neuroblastic tumor cells. The usually benign subtypes of peripheral neuroblastic tumors, i.e. ganglioneuroblastomas and ganglioneuromas, contain neuronal differentiating tumor cells and are pervaded by various portions of stromal SCs. Of note, the amount of stromal SCs correlates with a favorable tumor behavior and increased patient survival, whereas aggressive subtypes of peripheral neuroblastic tumors, i.e. neuroblastomas, usually lack stromal SCs and have bad prognosis. This enigma prompted us to investigate the molecular wiring and functional state of stromal SCs versus injury-associated repair SCs and how SC signals could be leveraged as therapeutics. ResultOur study revealed that the cellular state of stromal SCs in ganglioneuromas is in many aspects very similar to human repair SCs in injured nerves as both, stromal SCs and repair SCs, are equipped with distinct nerve repair-associated functions. Hence, we exposed different cell lines, derived from high-risk metastatic neuroblastomas, to primary repair SCs or their secretome. The results demonstrated that repair SCs had a pro-differentiating and anti-proliferative effect of on neuroblastoma cell lines upon direct and/or indirect contact. Searching for secreted anti-tumor factors by transcriptome and proteome analyses identified that the matricellular protein EGFL8 was highly expressed in injured nerves and ganglioneuromas. EGFL8 gene expression in peripheral neuroblastic tumors further correlated with increased patient survival. Indeed, treatment of neuroblastoma cell lines with recombinant EGFL8 promoted neuronal differentiation and present EGFL8 as a novel neuritogen. ImpactThese findings demonstrate that stromal SCs are equipped with the tools to exert nerve repair-associated functions on peripheral neuroblastic tumor cells and the tumor microenvironment. We further show that the pool of secreted stromal/repair SC molecules contains yet uncharacterized factors with a therapeutic potential for aggressive neuroblastomas. We conclude that the inherent plasticity (reactive/adaptive potential) of SCs is responsible for the development of usually benign ganglioneuroblastomas and ganglioneuromas and, thus, is of utmost interest to be exploited in future treatment approaches for aggressive neuroblastoma subtypes.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Weiss, T., Taschner-Mandl, S., Bileck, A., Rifatbegovic, F., Sorger, H., Kauer, M., Frech, C., Windhager, R., Gerner, C., Ambros, P. F., Ambros, I. M.. 2020-04-01. Schwann cell plasticity regulates neuroblastic tumor cell differentiation. https://doi.org/10.1101/2020.04.01.019422

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The methionine cycle sustains the mesenchymal phenotype of tumor cells and drives PDA progression

Mesenchymal traits are associated with poor prognosis in Pancreatic Ductal Adenocarcinoma (PDA), but direct targeting of mesenchymal tumor cells remains a challenge. Metabolic profiling of tumor cells isolated from murine PDA and liver metastases (LM) revealed that LM rely more on the methionine cycle than does primary PDA. This metabolic shift was specifically associated with increased activation of the methionine cycle in mesenchymal tumor cells compared to differentiated tumor cells. We show that the targeting of the key enzyme of the methionine cycle S-adenosylhomocysteine hydrolase (SAHH) in mesenchymal cells lowers the levels of homocysteine (Hcy) and glutathione, resulting in reduced antioxidant capacity, deregulated intracellular calcium homeostasis, and ultimately loss of mesenchymal markers. Together, these events decrease cell proliferation and invasion, blunting the tumorigenic and metastatic potential of SAHH-deficient cells, eventually impeding tumor growth and progression of the metastatic disease. Clinically, the high expression of SAHH in patients with mesenchymal PDA is correlated with poor survival, positioning SAHH as a potential therapeutic target to impede the pro-metastatic, mesenchymal phenotype of PDA.

cancer biology↗

Arrest-associated transcriptional programmes outweigh apoptosis-associated programmes in treatment-naive pancreatic ductal adenocarcinoma

Background: Pancreatic ductal adenocarcinoma (PDAC) is driven by mutant KRAS, and RAS inhibitors now extend survival in previously treated metastatic disease. Whether treatment shrinks a tumour or only halts its growth depends partly on whether cancer cells die or stop dividing, yet how untreated PDAC cells are balanced between these programmes is unknown. Aims: We aimed to characterise the balance between apoptosis-associated and arrest-associated transcriptional programmes in treatment-naive PDAC and to examine their relationships with tumour subtype, TGM2 expression, tissue organisation, survival and drug sensitivity. Methods and results: We scored 52,999 malignant cells from 18 untreated patients in the Hwang atlas using a transcriptional contrast between genes associated with apoptosis and genes associated with resistance to apoptosis or cell-cycle arrest. In every patient the contrast was shifted toward the arrest-associated side: using equality between the two sides as the dividing threshold, 86.3% of cells with an informative score fell on that side, although the proportion depends on the threshold chosen. The shift recurred in the independent Steele atlas (median 71.6% per sample, range 37.1% to 90.8%). In the discovery cohort, tumours with higher basal-like scores had fewer arrest-side cells, and TGM2 expression was modestly higher on the arrest-associated side in both cohorts. The contrast did not track cell-line drug sensitivity or survival in bulk tumours. Conclusion: Untreated PDAC cells show a reproducible transcriptional bias toward anti-apoptotic and cell-cycle-arrest programmes. Whether this bias predicts cellular responses to treatment remains to be tested.

cancer biology↗

Quantitative live imaging reveals region-dependent medulloblastoma disseminationin the zebrafish brain

Medulloblastoma is the most common malignant pediatric brain tumor, and relapse is frequently driven by dissemination within the central nervous system. Yet the early dynamics of tumor spread remain difficult to resolve in vivo. Here, we orthotopically transplanted human medulloblastoma cells into larval zebrafish and followed individual xenografts by longitudinal high-resolution confocal imaging. ONS-76 showed particularly robust dissemination, with hindbrain tumors spreading into the developing cerebellum in 81.5% of larvae, more than fourfold the frequency observed for forebrain or midbrain tumors. Disseminating cells extended along brain-surface and leptomeningeal-like regions and frequently associated with cerebral vasculature. Quantitative analysis of tumor area, perimeter, compactness, convex hull area, and fractal dimension captured changes in growth and spatial complexity over time. Dasatinib reduced tumor expansion and dissemination-related features in a concentration-dependent manner, while higher doses revealed host toxicity. These findings establish a powerful in vivo model for resolving medulloblastoma dissemination and therapeutic response.

cancer biology↗