N-myc and Noncoding RNAs in Neuroblastoma

Buechner, Jochen; Einvik, Christer

doi:10.1158/1541-7786.mcr-12-0244

Cited by 61 publications

(57 citation statements)

References 100 publications

(119 reference statements)

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“…In addition, N‐myc induced miRNA signature in human cancer involving the activation and trans‐repression of several miRNA genes from paralogous clusters 35, 36. We suspected that miR‐4295 is regulated by N‐myc in glioma.…”

Section: Discussionmentioning

confidence: 99%

RUNX3 is down‐regulated in glioma by Myc‐regulated miR‐4295

Zheng

Diao

et al. 2016

J Cellular Molecular Medi

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MicroRNAs are increasingly reported as tumour suppressors that regulate gene expression after transcription. Our results demonstrated that miR‐4295 is overexpression in glioma tissues and its level is significantly correlated with clinical stage. We also found that miR‐4295 inhibited the cell G0/G1 arrest and apoptosis leading to promoted cell proliferation and activity. The murine modelling study revealed that female nude mice injected with U87/anti‐miR‐4295 exhibit subcutaneous tumours in the right groin. Compared with anti‐NC, the tumour volume was significantly decreased in anti‐miR‐4295 treatment group. Furthermore, we confirmed miR‐4295 mediates the expression of RUNX3 by targeting its 3′untranslation region. In addition, N‐myc protein also could bind to the promoter of pri‐miR‐4295 and inhibit the expression of RUNX3 in glioma cells. These results validate a pathogenetic role of a miR‐4295 in gliomas and establish a potentially regulatory and signalling pathway involving N‐myc/miR‐4295/RUNX3 in gliomas.

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Section: Discussionmentioning

confidence: 99%

RUNX3 is down‐regulated in glioma by Myc‐regulated miR‐4295

Zheng

Diao

et al. 2016

J Cellular Molecular Medi

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“…In neuroblastoma, Nmyc can activate several microRNAs (mir-17-92, mir-221, mir-9, and mir-421) and long noncoding RNAs (T-UCRs and ncRAN) and repress others (mir-184 and mir-542-5p), which can contribute to the oncogenic phenotype through regulation of downstream pathways involved in apoptosis, differentiation, epithelial-to-mesenchymal transition, and DNA damage response (67). Furthermore, transcriptome profiling of N-myc-associated miRNAs in human neuroblastomas has demonstrated prognostic significance (68).…”

Section: Functional Targets Of N-mycmentioning

confidence: 99%

The N-myc Oncogene: Maximizing its Targets, Regulation, and Therapeutic Potential

Beltran

2014

Molecular Cancer Research

124

116

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N-myc (MYCN), a member of the Myc family of basic-helix-loop-helix-zipper (bHLHZ) transcription factors, is a central regulator of many vital cellular processes. As such, N-myc is well recognized for its classic oncogenic activity and association with human neuroblastoma. Amplification and overexpression of N-myc has been described in other tumor types, particularly those of neural origin and neuroendocrine tumors. This review outlines N-myc's contribution to normal development and oncogenic progression. In addition, it highlights relevant transcriptional targets and mechanisms of regulation. Finally, the clinical implications of N-Myc as a biomarker and potential as a target using novel therapeutic approaches are discussed. Mol Cancer Res; 12(6); 815-22. Ó2014 AACR. IntroductionThe N-myc gene was first reported in 1983, when Schwab and colleagues (1) and Kohl and colleagues (2) discovered that there were a subset of human neuroblastoma cell lines harboring multiple copies of a DNA sequence related to the C-myc oncogene (MYC), and this region was designated Nmyc (MYCN). Genomic amplification of N-myc resulted in overexpression of N-myc at the mRNA level, and rat embryo cells transfected with N-myc demonstrated oncogenic properties. These findings were first to bring attention to N-myc as a putative oncogene.

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“…26 These data suggest thac-Myb can have a role in the regulation of epithelial-mesenchymal transition of some tumor types. 27,28 There are examples of the interplay between oncogenes and miRNAs in controlling central events in tumor progression and metastasis, 29,30 but the complete picture of these interactions is far from being complete.…”

Section: Introductionmentioning

confidence: 99%

Activation of miR200 by c-Myb depends on ZEB1 expression and miR200 promoter methylation

et al. 2013

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RepoRt tumor progression to metastasis is a complex, sequential process that requires proliferation, resistance to apoptosis, motility and invasion to colonize at distant sites. the acquisition of these features implies a phenotypic plasticity by tumor cells that must adapt to different conditions by modulating several signaling pathways 1 during the journey to the final site of metastasis. Several transcription factors and microRNA play a role in tumor progression, but less is known about the control of their expression during this process. Here, we demonstrate by ectopic expression and gene silencing that the proto-oncogene c-Myb activates the expression of the five members of miR200 family (miR200b, miR200a, miR429, miR200c and miR141) that are involved in the control of epithelial-mesenchymal transition (eMt) and metastasis in many types of cancers. transcriptional activation of miR200 by c-Myb occurs through binding to myb binding sites located in the promoter regions of miR200 genes on human chromosomes 1 and 12. Furthermore, when c-Myb and the transcriptional repressor ZeB1 are co-expressed, as at the onset eMt, the repression by ZeB1 prevails over the activation by c-Myb, and the expression of miR200 is inhibited. We also demonstrate that during eMt induced by tGF-b, the promoters of miR200 genes are methylated, and their transcription is repressed regardless of the presence of repressors such as ZeB1 and activators such as c-Myb. Finally, we find a correlation between the expression of c-Myb and that of four out of five miR200 in a data set of 207 breast cancer patients.

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N-myc and Noncoding RNAs in Neuroblastoma

Cited by 61 publications

References 100 publications

RUNX3 is down‐regulated in glioma by Myc‐regulated miR‐4295

RUNX3 is down‐regulated in glioma by Myc‐regulated miR‐4295

The N-myc Oncogene: Maximizing its Targets, Regulation, and Therapeutic Potential

Activation of miR200 by c-Myb depends on ZEB1 expression and miR200 promoter methylation

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