The low affinity neurotrophin receptor CD271 regulates phenotype switching in melanoma

Gaetana Restivo, Johanna Diener, Phil F. Cheng, Gregor Kiowski, Mario Bonalli, Thomas Biedermann, Ernst Reichmann, Mitchell P. Levesque, Reinhard Dummer and Lukas Sommer ()
Additional contact information
Gaetana Restivo: University of Zürich, Institute of Anatomy
Johanna Diener: University of Zürich, Institute of Anatomy
Phil F. Cheng: University of Zürich Hospital, Department of Dermatology
Gregor Kiowski: University of Zürich, Institute of Anatomy
Mario Bonalli: University of Zürich, Institute of Anatomy
Thomas Biedermann: University of Zürich Children’s Hospital, Tissue Biology Research Unit
Ernst Reichmann: University of Zürich Hospital, Department of Dermatology
Mitchell P. Levesque: University of Zürich Hospital, Department of Dermatology
Reinhard Dummer: University of Zürich Hospital, Department of Dermatology
Lukas Sommer: University of Zürich, Institute of Anatomy

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract Cutaneous melanoma represents the most fatal skin cancer due to its high metastatic capacity. According to the “phenotype switching” model, the aggressive nature of melanoma cells results from their intrinsic potential to dynamically switch from a high-proliferative/low-invasive to a low-proliferative/high-invasive state. Here we identify the low affinity neurotrophin receptor CD271 as a key effector of phenotype switching in melanoma. CD271 plays a dual role in this process by decreasing proliferation, while simultaneously promoting invasiveness. Dynamic modification of CD271 expression allows tumor cells to grow at low levels of CD271, to reduce growth and invade when CD271 expression is high, and to re-expand at a distant site upon decrease of CD271 expression. Mechanistically, the cleaved intracellular domain of CD271 controls proliferation, while the interaction of CD271 with the neurotrophin receptor Trk-A modulates cell adhesiveness through dynamic regulation of a set of cholesterol synthesis genes relevant for patient survival.

Date: 2017
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-017-01573-6 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:8:y:2017:i:1:d:10.1038_s41467-017-01573-6

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

DOI: 10.1038/s41467-017-01573-6

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 ().