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...

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Bibliographic Details
Published inCancers Vol. 12; no. 9; p. 2460
Main Authors Vidal, Anna, Redmer, Torben
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.09.2020
MDPI
Subjects
Ablation
Antigens
CD271
Cell adhesion & migration
Cell cycle
Cell migration
Coding
Fibrosarcoma
Genotype & phenotype
Growth factors
Invasiveness
Melanocytes
Melanoma
Metastases
Metastasis
migration
Mutation
Neural crest
neural crest stem cells
Neuroblastoma
Phenotypes
Physiological aspects
Protein-serine/threonine kinase
Review
Senescence
Skin cancer
Stem cell transplantation
Stem cells
Therapeutic applications
Tumors
United States
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Summary: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.
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ISSN:2072-6694
2072-6694
DOI:10.3390/cancers12092460