MYCN

Official Full Name

MYCN proto-oncogene, bHLH transcription factor

Organism

Homo sapiens

GeneID

4613

Background

This gene is a member of the MYC family and encodes a protein with a basic helix-loop-helix (bHLH) domain. This protein is located in the nucleus and must dimerize with another bHLH protein in order to bind DNA. Amplification of this gene is associated with a variety of tumors, most notably neuroblastomas. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jun 2014]

Synonyms

NMYC; ODED; MODED; MPAPA; N-myc; FGLDS1; bHLHe37; MYCNsORF; MYCNsPEP;

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Detailed Information

The most characteristic genes in the MYC multigene family are c-MYC, L-MYC, and MYCN (N-MYC). MYCN is located in the chromosome 2p24 region, and the gene sequences of MYCN and c-MYC are structurally broadly homologous, and protein function and biochemical characteristics are closely related. However, the expression of MYCN is mainly in the nervous system and interstitial tissues, especially in the embryonic stage.

There are miRNAs in almost every organism. Since miRNAs can target many different mRNAs, each mRNA may contain several to hundreds of miRNA binding sites. Obviously, the miRNA-mRNA regulatory network is extremely Complex, it is involved in proliferation, differentiation, signaling, apoptosis and immune defense. miRNAs play an important role in the process of complex diseases, and may also have carcinogenic and tumor suppressive effects. The transcription of miRNAs is regulated by several transcription factors, including the pro-oncogene c-MYC, MYCN, and the tumor suppressor gene TP53.

The Role of MYCN

In addition to neuroblastoma, MYCN is also expressed in other embryos or endocrine-derived tumors such as retinoblastoma, Wlims' tumor, rhabdomyosarcoma, medulloblastoma, glioblastoma, and small cell lung cancer. Like other proteins in the MYC family, MYCN is also a transcription factor that regulates the expression of multiple genes of interest, thereby regulating cellular functions such as cell proliferation, cell growth, protein synthesis, cellular metabolism, cell invasion and metastasis, and apoptosis. 25% to 30% of children with neuroblastoma have MYCN gene amplification, and many children with advanced stage have poor therapeutic effect and poor pre-exposure. About 40% of high-risk neuroblastomas are highly expressed in MYCN. The consistent high expression of MYCN was detected in neuroblastoma tissues from different sites or at different periods from diagnosis to recurrence, suggesting that the high expression of MYCN is a stable and inherent characteristic of neuroblastoma with high risk.

Figure 1. Strategies for direct and indirect targeting of MYCN. (Ruiz-Pérez María Victoria, et al. 2017)

MYCN and Neuroblastoma

Cell proliferation is a process in which the number of cells is increased by cell-to-peer division to produce daughter cells having the same genetic characteristics as the mother cells. Overexpression of MYCN promotes proliferation of neuroblastoma cells. The study confirmed in nude mice that NLLRR1 enhances EGF-mediated proliferation of MY-CN-induced neuroblastoma. At present, there is a lot of evidence that MYCN is associated with apoptosis of neuroblastoma cells. After experimentally inducing MYCN overexpression, it mainly promotes cell apoptosis through the ARF/p53 pathway. In vitro NB cells were infected with small interfering (si) RNA, and the expression of MYCN was decreased to induce apoptosis, thereby inhibiting the growth of neuroblastoma cells. Both in vitro and in vivo experiments demonstrated that GANT61 can induce apoptosis of neuroblastoma after decreasing the expression of GLI1, c-MYC and MYCN mRNA in Hedgehog (HH) signaling pathway.

Angiogenesis factor (VEGF) plays an important role in angiogenesis. It was found that PI3K inhibitor wortmannin was used in cells with high expression of MYCN. After that, the expression of MYCN is decreased; and siRNA interfering with the expression of MYCN blocks the secretion of VEGF. The study also found that PI3K, which regulates angiogenesis in neuroblastoma, was reduced by the addition of the PI3K inhibitor NVP-BEZ235, resulting in reduced angiogenesis in neuroblastoma. The study found that angiogenin (ANG) plays an important role in angiogenesis in neuroblastoma, and ANG is closely related to the prognosis of patients with neuroblastoma clinical pathology and cell biology, while ANG is 4 Significant increase in neuroblastoma and MYCN overexpression.

References:

Ruiz-Pérez María Victoria, Brigette, H. A. , & Marie, A. H. . (2017). The mycn protein in health and disease. Genes, 8(4), 113-.
Vaughan, L. , Clarke, P. A. , Barker, K. , Chanthery, Y. , & Chesler, L. . (2016). Inhibition of mtor-kinase destabilizes mycn and is a potential therapy for mycn-dependent tumors. Oncotarget, 7(36), 57525-57544.
Hsu, C. L. , Chang, H. Y. , Chang, J. Y. , Hsu, W. M. , Huang, H. C. , & Juan, H. F. . (2016). Unveiling mycn regulatory networks in neuroblastoma via integrative analysis of heterogeneous genomics data. Oncotarget, 7(24), 36293-36310.

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