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Targeting the epigenome of cancer stem cells in pediatric nervous system tumors
Medulloblastoma, neuroblastoma, and pediatric glioma account for almost 30% of all cases of pediatric cancers. Recent evidence indicates that pediatric nervous system tumors originate from stem or progenitor cells and present a subpopulation of cells with highly tumorigenic and stem cell-like featur...
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| Published in: | Molecular and cellular biochemistry 2023-10, Vol.478 (10), p.2241-2255 |
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| container_title | Molecular and cellular biochemistry |
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| creator | Freire, Natália Hogetop Jaeger, Mariane da Cunha de Farias, Caroline Brunetto Nör, Carolina Souza, Barbara Kunzler Gregianin, Lauro Brunetto, André Tesainer Roesler, Rafael |
| description | Medulloblastoma, neuroblastoma, and pediatric glioma account for almost 30% of all cases of pediatric cancers. Recent evidence indicates that pediatric nervous system tumors originate from stem or progenitor cells and present a subpopulation of cells with highly tumorigenic and stem cell-like features. These cancer stem cells play a role in initiation, progression, and resistance to treatment of pediatric nervous system tumors. Histone modification, DNA methylation, chromatin remodeling, and microRNA regulation display a range of regulatory activities involved in cancer origin and progression, and cellular identity, especially those associated with stem cell features, such as self-renewal and pluripotent differentiation potential. Here, we review the contribution of different epigenetic mechanisms in pediatric nervous system tumor cancer stem cells. The choice between a differentiated and undifferentiated state can be modulated by alterations in the epigenome through the regulation of stemness genes such as CD133, SOX2, and BMI1 and the activation neuronal of differentiation markers, RBFOX3, GFAP, and S100B. Additionally, we highlighted the stage of development of epigenetic drugs and the clinical benefits and efficacy of epigenetic modulators in pediatric nervous system tumors. |
| doi_str_mv | 10.1007/s11010-022-04655-2 |
| format | article |
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Recent evidence indicates that pediatric nervous system tumors originate from stem or progenitor cells and present a subpopulation of cells with highly tumorigenic and stem cell-like features. These cancer stem cells play a role in initiation, progression, and resistance to treatment of pediatric nervous system tumors. Histone modification, DNA methylation, chromatin remodeling, and microRNA regulation display a range of regulatory activities involved in cancer origin and progression, and cellular identity, especially those associated with stem cell features, such as self-renewal and pluripotent differentiation potential. Here, we review the contribution of different epigenetic mechanisms in pediatric nervous system tumor cancer stem cells. The choice between a differentiated and undifferentiated state can be modulated by alterations in the epigenome through the regulation of stemness genes such as CD133, SOX2, and BMI1 and the activation neuronal of differentiation markers, RBFOX3, GFAP, and S100B. Additionally, we highlighted the stage of development of epigenetic drugs and the clinical benefits and efficacy of epigenetic modulators in pediatric nervous system tumors.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-022-04655-2</identifier><identifier>PMID: 36637615</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Amino acids ; Biochemistry ; Biomedical and Life Sciences ; Brain cancer ; Brain tumors ; Cancer ; Cancer Research ; Cardiology ; Cell differentiation ; Cell self-renewal ; Chromatin ; Chromatin remodeling ; Development and progression ; Developmental stages ; Differentiation ; DNA methylation ; Drug development ; Epigenetic inheritance ; Epigenetics ; Gene regulation ; Genes ; Glial fibrillary acidic protein ; Glioma ; Gliomas ; Histones ; Life Sciences ; Medical Biochemistry ; Medulloblastoma ; Methylation ; MicroRNA ; miRNA ; Modulators ; Nervous system ; Nervous system tumors ; Neural stem cells ; Neuroblastoma ; Neuromodulation ; Neurophysiology ; Pediatrics ; Pluripotency ; Progenitor cells ; Ribonucleic acid ; RNA ; S100b protein ; Stem cell research ; Stem cells ; Tumors ; Vorinostat</subject><ispartof>Molecular and cellular biochemistry, 2023-10, Vol.478 (10), p.2241-2255</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>COPYRIGHT 2023 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-3ad9f2520fb06ad8a42654301f72f0d8d62642a32c38ed8da0dc00878287975c3</citedby><cites>FETCH-LOGICAL-c442t-3ad9f2520fb06ad8a42654301f72f0d8d62642a32c38ed8da0dc00878287975c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36637615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Freire, Natália Hogetop</creatorcontrib><creatorcontrib>Jaeger, Mariane da Cunha</creatorcontrib><creatorcontrib>de Farias, Caroline Brunetto</creatorcontrib><creatorcontrib>Nör, Carolina</creatorcontrib><creatorcontrib>Souza, Barbara Kunzler</creatorcontrib><creatorcontrib>Gregianin, Lauro</creatorcontrib><creatorcontrib>Brunetto, André Tesainer</creatorcontrib><creatorcontrib>Roesler, Rafael</creatorcontrib><title>Targeting the epigenome of cancer stem cells in pediatric nervous system tumors</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Medulloblastoma, neuroblastoma, and pediatric glioma account for almost 30% of all cases of pediatric cancers. Recent evidence indicates that pediatric nervous system tumors originate from stem or progenitor cells and present a subpopulation of cells with highly tumorigenic and stem cell-like features. These cancer stem cells play a role in initiation, progression, and resistance to treatment of pediatric nervous system tumors. Histone modification, DNA methylation, chromatin remodeling, and microRNA regulation display a range of regulatory activities involved in cancer origin and progression, and cellular identity, especially those associated with stem cell features, such as self-renewal and pluripotent differentiation potential. Here, we review the contribution of different epigenetic mechanisms in pediatric nervous system tumor cancer stem cells. The choice between a differentiated and undifferentiated state can be modulated by alterations in the epigenome through the regulation of stemness genes such as CD133, SOX2, and BMI1 and the activation neuronal of differentiation markers, RBFOX3, GFAP, and S100B. Additionally, we highlighted the stage of development of epigenetic drugs and the clinical benefits and efficacy of epigenetic modulators in pediatric nervous system tumors.</description><subject>Amino acids</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cell differentiation</subject><subject>Cell self-renewal</subject><subject>Chromatin</subject><subject>Chromatin remodeling</subject><subject>Development and progression</subject><subject>Developmental stages</subject><subject>Differentiation</subject><subject>DNA methylation</subject><subject>Drug development</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Gene regulation</subject><subject>Genes</subject><subject>Glial fibrillary acidic protein</subject><subject>Glioma</subject><subject>Gliomas</subject><subject>Histones</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Medulloblastoma</subject><subject>Methylation</subject><subject>MicroRNA</subject><subject>miRNA</subject><subject>Modulators</subject><subject>Nervous system</subject><subject>Nervous system tumors</subject><subject>Neural stem cells</subject><subject>Neuroblastoma</subject><subject>Neuromodulation</subject><subject>Neurophysiology</subject><subject>Pediatrics</subject><subject>Pluripotency</subject><subject>Progenitor cells</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>S100b protein</subject><subject>Stem cell research</subject><subject>Stem 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Recent evidence indicates that pediatric nervous system tumors originate from stem or progenitor cells and present a subpopulation of cells with highly tumorigenic and stem cell-like features. These cancer stem cells play a role in initiation, progression, and resistance to treatment of pediatric nervous system tumors. Histone modification, DNA methylation, chromatin remodeling, and microRNA regulation display a range of regulatory activities involved in cancer origin and progression, and cellular identity, especially those associated with stem cell features, such as self-renewal and pluripotent differentiation potential. Here, we review the contribution of different epigenetic mechanisms in pediatric nervous system tumor cancer stem cells. 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| subjects | Amino acids Biochemistry Biomedical and Life Sciences Brain cancer Brain tumors Cancer Cancer Research Cardiology Cell differentiation Cell self-renewal Chromatin Chromatin remodeling Development and progression Developmental stages Differentiation DNA methylation Drug development Epigenetic inheritance Epigenetics Gene regulation Genes Glial fibrillary acidic protein Glioma Gliomas Histones Life Sciences Medical Biochemistry Medulloblastoma Methylation MicroRNA miRNA Modulators Nervous system Nervous system tumors Neural stem cells Neuroblastoma Neuromodulation Neurophysiology Pediatrics Pluripotency Progenitor cells Ribonucleic acid RNA S100b protein Stem cell research Stem cells Tumors Vorinostat |
| title | Targeting the epigenome of cancer stem cells in pediatric nervous system tumors |
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