MYCN as an oncogene in pediatric brain tumors

MYCN, or N-Myc, is a member of the MYC family of transcription factors, which plays a key role in tumor formation by regulating genes involved in proliferation, differentiation, and apoptosis. MYCN is essential for neural development, especially for the appropriate growth and differentiation of neur...

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Main Authors: Adriana Fernandez Garcia, Jayden Jackson, Poorvi Iyer, Elissa G. Oliver, Kosuke Funato
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-04-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2025.1584978/full
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author Adriana Fernandez Garcia
Adriana Fernandez Garcia
Jayden Jackson
Jayden Jackson
Poorvi Iyer
Poorvi Iyer
Elissa G. Oliver
Elissa G. Oliver
Kosuke Funato
Kosuke Funato
author_facet Adriana Fernandez Garcia
Adriana Fernandez Garcia
Jayden Jackson
Jayden Jackson
Poorvi Iyer
Poorvi Iyer
Elissa G. Oliver
Elissa G. Oliver
Kosuke Funato
Kosuke Funato
author_sort Adriana Fernandez Garcia
collection DOAJ
description MYCN, or N-Myc, is a member of the MYC family of transcription factors, which plays a key role in tumor formation by regulating genes involved in proliferation, differentiation, and apoptosis. MYCN is essential for neural development, especially for the appropriate growth and differentiation of neural progenitor cells, and its aberrant expression contributes to tumorigenesis. Gene amplification and mutations of this gene have been observed in a wide variety of cancer types, particularly in pediatric brain and non-brain tumors, such as neuroblastoma. Previous studies have provided extensive insights into the complex regulatory network of this transcription factor. Additionally, the presence of MYCN alterations in patient tumors serve as a key factor for risk stratification, as it correlates with poorer outcomes, and presents a significant challenge for treatment. Despite its clinical significance, therapeutic targeting of MYCN is challenging due to its structure, nuclear localization, and complex regulatory pathways. Efforts to target MYCN have focused on destabilizing the protein, modulating epigenetic mechanisms, and disrupting its transcriptional network. This review explores the role of MYCN in different subtypes of pediatric brain tumors and highlights novel ongoing therapeutic approaches. However, further research is necessary to develop more effective therapies and improve survival outcomes for patients with MYCN-driven tumor.
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spelling doaj-art-ec550e7a19cb49428743b71e85a830bb2025-08-20T03:53:27ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2025-04-011510.3389/fonc.2025.15849781584978MYCN as an oncogene in pediatric brain tumorsAdriana Fernandez Garcia0Adriana Fernandez Garcia1Jayden Jackson2Jayden Jackson3Poorvi Iyer4Poorvi Iyer5Elissa G. Oliver6Elissa G. Oliver7Kosuke Funato8Kosuke Funato9Center for Molecular Medicine, University of Georgia, Athens, GA, United StatesDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, United StatesCenter for Molecular Medicine, University of Georgia, Athens, GA, United StatesDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, United StatesCenter for Molecular Medicine, University of Georgia, Athens, GA, United StatesDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, United StatesCenter for Molecular Medicine, University of Georgia, Athens, GA, United StatesDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, United StatesCenter for Molecular Medicine, University of Georgia, Athens, GA, United StatesDepartment of Biochemistry and Molecular Biology, University of Georgia, Athens, GA, United StatesMYCN, or N-Myc, is a member of the MYC family of transcription factors, which plays a key role in tumor formation by regulating genes involved in proliferation, differentiation, and apoptosis. MYCN is essential for neural development, especially for the appropriate growth and differentiation of neural progenitor cells, and its aberrant expression contributes to tumorigenesis. Gene amplification and mutations of this gene have been observed in a wide variety of cancer types, particularly in pediatric brain and non-brain tumors, such as neuroblastoma. Previous studies have provided extensive insights into the complex regulatory network of this transcription factor. Additionally, the presence of MYCN alterations in patient tumors serve as a key factor for risk stratification, as it correlates with poorer outcomes, and presents a significant challenge for treatment. Despite its clinical significance, therapeutic targeting of MYCN is challenging due to its structure, nuclear localization, and complex regulatory pathways. Efforts to target MYCN have focused on destabilizing the protein, modulating epigenetic mechanisms, and disrupting its transcriptional network. This review explores the role of MYCN in different subtypes of pediatric brain tumors and highlights novel ongoing therapeutic approaches. However, further research is necessary to develop more effective therapies and improve survival outcomes for patients with MYCN-driven tumor.https://www.frontiersin.org/articles/10.3389/fonc.2025.1584978/fullMYCNpediatric brain tumorstumorigenesisoncogeneneuro-oncology
spellingShingle Adriana Fernandez Garcia
Adriana Fernandez Garcia
Jayden Jackson
Jayden Jackson
Poorvi Iyer
Poorvi Iyer
Elissa G. Oliver
Elissa G. Oliver
Kosuke Funato
Kosuke Funato
MYCN as an oncogene in pediatric brain tumors
Frontiers in Oncology
MYCN
pediatric brain tumors
tumorigenesis
oncogene
neuro-oncology
title MYCN as an oncogene in pediatric brain tumors
title_full MYCN as an oncogene in pediatric brain tumors
title_fullStr MYCN as an oncogene in pediatric brain tumors
title_full_unstemmed MYCN as an oncogene in pediatric brain tumors
title_short MYCN as an oncogene in pediatric brain tumors
title_sort mycn as an oncogene in pediatric brain tumors
topic MYCN
pediatric brain tumors
tumorigenesis
oncogene
neuro-oncology
url https://www.frontiersin.org/articles/10.3389/fonc.2025.1584978/full
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