About this Research Topic
MYCN encodes a transcription factor that functions as an oncoprotein, similar to the other MYC family proteins, c-MYC and L-Myc. Since its discovery as an amplified gene homologous to c-MYC in neuroblastoma, MYCN has been found to be amplified and overexpressed in various tumors, including glioblastoma, medulloblastoma, retinoblastoma, abdominal tumors, Wilms tumors, acute myeloid leukemia, small cell lung carcinomas, breast cancers, and prostate cancers.
MYCN is always co-amplified with the cis-antisense transcript of MYCN (MYCNOS or NCYM) that induces MYCN expression at both protein and RNA levels. Moreover, the long noncoding RNA (lncRNA) located upstream of MYCN stimulates MYCN transcription. These transcripts directly or indirectly enhance MYCN expression, contributing to tumorigenesis. In addition to the amplification, dysfunction of transcriptional regulation also results in the overexpression of MYCN. MYCN promotes tumor aggressiveness by orchestrating cell proliferation, differentiation, stemness, and metabolism via transcription-dependent or -independent mechanisms.
Until recently, the MYCN structure was thought to be undruggable; however, recent studies have revealed methods to target this oncogene by acting on its transcription, stability and downstream signaling. These treatments have achieved improved prognosis in clinical trials; however, the standard therapy for MYCN-driven tumors needs to be established. This topic focuses on the function/regulation(s) of MYCN in tumorigenesis and novel approaches for the treatment of MYCN-driven tumors. We welcome Original Research and Review articles focusing on, but not limited to:
1) The role of MYCN in carcinogenesis and research on carcinogenesis as a failure of the physiological function of MYCN. This includes research to establish new experimental systems and animal models that study and explain the functions of MYCN.
2) Novel functions of MYCN in tumor progression, i.e., in metastasis or drug resistance.
3) Transcription-independent mechanism of MYCN-driven tumorigenesis.
4) Development of drugs and diagnostic methods for MYCN-driven tumors. This topic also covers the development of new drugs and the improvement of existing drugs that target the upstream regulation of MYCN, downstream genes, binding factors, and the MYCN gene itself.
5) Research on the evolution of the regulatory mechanisms of MYCN and analysis of species-specific downstream target genes, such as lncRNA.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
MYCN is always co-amplified with the cis-antisense transcript of MYCN (MYCNOS or NCYM) that induces MYCN expression at both protein and RNA levels. Moreover, the long noncoding RNA (lncRNA) located upstream of MYCN stimulates MYCN transcription. These transcripts directly or indirectly enhance MYCN expression, contributing to tumorigenesis. In addition to the amplification, dysfunction of transcriptional regulation also results in the overexpression of MYCN. MYCN promotes tumor aggressiveness by orchestrating cell proliferation, differentiation, stemness, and metabolism via transcription-dependent or -independent mechanisms.
Until recently, the MYCN structure was thought to be undruggable; however, recent studies have revealed methods to target this oncogene by acting on its transcription, stability and downstream signaling. These treatments have achieved improved prognosis in clinical trials; however, the standard therapy for MYCN-driven tumors needs to be established. This topic focuses on the function/regulation(s) of MYCN in tumorigenesis and novel approaches for the treatment of MYCN-driven tumors. We welcome Original Research and Review articles focusing on, but not limited to:
1) The role of MYCN in carcinogenesis and research on carcinogenesis as a failure of the physiological function of MYCN. This includes research to establish new experimental systems and animal models that study and explain the functions of MYCN.
2) Novel functions of MYCN in tumor progression, i.e., in metastasis or drug resistance.
3) Transcription-independent mechanism of MYCN-driven tumorigenesis.
4) Development of drugs and diagnostic methods for MYCN-driven tumors. This topic also covers the development of new drugs and the improvement of existing drugs that target the upstream regulation of MYCN, downstream genes, binding factors, and the MYCN gene itself.
5) Research on the evolution of the regulatory mechanisms of MYCN and analysis of species-specific downstream target genes, such as lncRNA.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Keywords: MYCN, carcinogenesis, transcription, treatment, evolution
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
