Mechanisms involved in selecting and maintaining neuroblastoma cancer stem cell populations, and perspectives for therapeutic targeting.
Cancer stem cells
Neural crest
Neuroblastoma
Polyploid giant cancer cells molecular mechanisms
Therapeutic targeting
Tumour microenvironment
Journal
World journal of stem cells
ISSN: 1948-0210
Titre abrégé: World J Stem Cells
Pays: United States
ID NLM: 101535826
Informations de publication
Date de publication:
26 Jul 2021
26 Jul 2021
Historique:
received:
27
01
2021
revised:
09
03
2021
accepted:
14
04
2021
entrez:
9
8
2021
pubmed:
10
8
2021
medline:
10
8
2021
Statut:
ppublish
Résumé
Pediatric neuroblastomas (NBs) are heterogeneous, aggressive, therapy-resistant embryonal tumours that originate from cells of neural crest (NC) origin and in particular neuroblasts committed to the sympathoadrenal progenitor cell lineage. Therapeutic resistance, post-therapeutic relapse and subsequent metastatic NB progression are driven primarily by cancer stem cell (CSC)-like subpopulations, which through their self-renewing capacity, intermittent and slow cell cycles, drug-resistant and reversibly adaptive plastic phenotypes, represent the most important obstacle to improving therapeutic outcomes in unfavourable NBs. In this review, dedicated to NB CSCs and the prospects for their therapeutic eradication, we initiate with brief descriptions of the unique transient vertebrate embryonic NC structure and salient molecular protagonists involved NC induction, specification, epithelial to mesenchymal transition and migratory behaviour, in order to familiarise the reader with the embryonic cellular and molecular origins and background to NB. We follow this by introducing NB and the potential NC-derived stem/progenitor cell origins of NBs, before providing a comprehensive review of the salient molecules, signalling pathways, mechanisms, tumour microenvironmental and therapeutic conditions involved in promoting, selecting and maintaining NB CSC subpopulations, and that underpin their therapy-resistant, self-renewing metastatic behaviour. Finally, we review potential therapeutic strategies and future prospects for targeting and eradication of these bastions of NB therapeutic resistance, post-therapeutic relapse and metastatic progression.
Identifiants
pubmed: 34367474
doi: 10.4252/wjsc.v13.i7.685
pmc: PMC8316860
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
685-736Informations de copyright
©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflict-of-interest statement: The authors of this manuscript declare no conflicts of interest.
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