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

Tamara Weiss, Sabine Taschner-Mandl (), Lukas Janker, Andrea Bileck, Fikret Rifatbegovic, Florian Kromp, Helena Sorger, Maximilian O. Kauer, Christian Frech, Reinhard Windhager, Christopher Gerner, Peter F. Ambros and Inge M. Ambros
Additional contact information
Tamara Weiss: St. Anna Children’s Cancer Research Institute (CCRI)
Sabine Taschner-Mandl: St. Anna Children’s Cancer Research Institute (CCRI)
Lukas Janker: University of Vienna
Andrea Bileck: University of Vienna
Fikret Rifatbegovic: St. Anna Children’s Cancer Research Institute (CCRI)
Florian Kromp: St. Anna Children’s Cancer Research Institute (CCRI)
Helena Sorger: St. Anna Children’s Cancer Research Institute (CCRI)
Maximilian O. Kauer: St. Anna Children’s Cancer Research Institute (CCRI)
Christian Frech: St. Anna Children’s Cancer Research Institute (CCRI)
Reinhard Windhager: Medical University of Vienna
Christopher Gerner: University of Vienna
Peter F. Ambros: St. Anna Children’s Cancer Research Institute (CCRI)
Inge M. Ambros: St. Anna Children’s Cancer Research Institute (CCRI)

Nature Communications, 2021, vol. 12, issue 1, 1-19

Abstract: Abstract 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.

Date: 2021
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-021-21859-0 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-21859-0

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-021-21859-0

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().