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Decoding the Role of CD271 in Melanoma
The evolution of melanoma, the most aggressive type of skin cancer, is triggered by driver mutations that are acquired in the coding regions of particularly BRAF (rat fibrosarcoma serine/threonine kinase, isoform B) or NRAS (neuroblastoma-type ras sarcoma virus) in melanocytes. Although driver mutat...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564075/ https://www.ncbi.nlm.nih.gov/pubmed/32878000 http://dx.doi.org/10.3390/cancers12092460 |
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author | Vidal, Anna Redmer, Torben |
author_facet | Vidal, Anna Redmer, Torben |
author_sort | Vidal, Anna |
collection | PubMed |
description | The evolution of melanoma, the most aggressive type of skin cancer, is triggered by driver mutations that are acquired in the coding regions of particularly BRAF (rat fibrosarcoma serine/threonine kinase, isoform B) or NRAS (neuroblastoma-type ras sarcoma virus) in melanocytes. Although driver mutations strongly determine tumor progression, additional factors are likely required and prerequisite for melanoma formation. Melanocytes are formed during vertebrate development in a well-controlled differentiation process of multipotent neural crest stem cells (NCSCs). However, mechanisms determining the properties of melanocytes and melanoma cells are still not well understood. The nerve growth factor receptor CD271 is likewise expressed in melanocytes, melanoma cells and NCSCs and programs the maintenance of a stem-like and migratory phenotype via a comprehensive network of associated genes. Moreover, CD271 regulates phenotype switching, a process that enables the rapid and reversible conversion of proliferative into invasive or non-stem-like states into stem-like states by yet largely unknown mechanisms. Here, we summarize current findings about CD271-associated mechanisms in melanoma cells and illustrate the role of CD271 for melanoma cell migration and metastasis, phenotype-switching, resistance to therapeutic interventions, and the maintenance of an NCSC-like state. |
format | Online Article Text |
id | pubmed-7564075 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75640752020-10-27 Decoding the Role of CD271 in Melanoma Vidal, Anna Redmer, Torben Cancers (Basel) Review The evolution of melanoma, the most aggressive type of skin cancer, is triggered by driver mutations that are acquired in the coding regions of particularly BRAF (rat fibrosarcoma serine/threonine kinase, isoform B) or NRAS (neuroblastoma-type ras sarcoma virus) in melanocytes. Although driver mutations strongly determine tumor progression, additional factors are likely required and prerequisite for melanoma formation. Melanocytes are formed during vertebrate development in a well-controlled differentiation process of multipotent neural crest stem cells (NCSCs). However, mechanisms determining the properties of melanocytes and melanoma cells are still not well understood. The nerve growth factor receptor CD271 is likewise expressed in melanocytes, melanoma cells and NCSCs and programs the maintenance of a stem-like and migratory phenotype via a comprehensive network of associated genes. Moreover, CD271 regulates phenotype switching, a process that enables the rapid and reversible conversion of proliferative into invasive or non-stem-like states into stem-like states by yet largely unknown mechanisms. Here, we summarize current findings about CD271-associated mechanisms in melanoma cells and illustrate the role of CD271 for melanoma cell migration and metastasis, phenotype-switching, resistance to therapeutic interventions, and the maintenance of an NCSC-like state. MDPI 2020-08-31 /pmc/articles/PMC7564075/ /pubmed/32878000 http://dx.doi.org/10.3390/cancers12092460 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Vidal, Anna Redmer, Torben Decoding the Role of CD271 in Melanoma |
title | Decoding the Role of CD271 in Melanoma |
title_full | Decoding the Role of CD271 in Melanoma |
title_fullStr | Decoding the Role of CD271 in Melanoma |
title_full_unstemmed | Decoding the Role of CD271 in Melanoma |
title_short | Decoding the Role of CD271 in Melanoma |
title_sort | decoding the role of cd271 in melanoma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564075/ https://www.ncbi.nlm.nih.gov/pubmed/32878000 http://dx.doi.org/10.3390/cancers12092460 |
work_keys_str_mv | AT vidalanna decodingtheroleofcd271inmelanoma AT redmertorben decodingtheroleofcd271inmelanoma |