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Review
. 2009;15(4):456-62.
doi: 10.2174/138161209787315837.

MicroRNA involvement in the pathogenesis of neuroblastoma: potential for microRNA mediated therapeutics

R L Stallings  1
Affiliations
Review

MicroRNA involvement in the pathogenesis of neuroblastoma: potential for microRNA mediated therapeutics

R L Stallings. Curr Pharm Des. 2009.

Abstract

Neuroblastoma arises from precursor cells of the sympathetic nervous system and presently accounts for 15% of all childhood cancer deaths. These tumors display remarkable heterogeneity in clinical behavior, ranging from spontaneous regression to rapid progression and resistance to therapy. The clinical behavior of these tumors is associated with many factors, including patient age, histopathology and genetic abnormalities such as MYCN amplification. More recently, the dysregulation of some miRNAs, including the miR-17-5p-92 cluster and miR-34a, has been implicated in the pathobiology of neuroblastoma. MiR-17-5p-92 family members act in an oncogenic manner while miR-34a has tumor suppressor functions VSports手机版. The evidence for the contribution of miRNAs in the aggressive neuroblastoma phenotype is reviewed in this article, along with exciting possibilities for miRNA mediated therapeutics. .

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Figures

Fig. (1)
Fig. (1)
Heat map summarizing the patterns of expression for 32 miRNA loci that were differentially expressed in neuroblastoma tumor subtypes (low stage hyperdiploid tumors with favorable histopathology, yellow; high stage 11q-tumors with unfavorable histopathology, pink; and high stage MYCN amplified tumors with unfavorable histopathology, blue). High expression is indicated by red, while low expression is indicated by green. MYCN amplified tumors form a distinct cluster characterized by low expression levels of many miRNA loci. The 11q- tumors formed two separate clusters, which could not always be perfectly distinguished from the low stage hyperdiploid tumors. This figure and its legend was originally published by Chen and Stallings [19] in Cancer Research and is reproduced here with the permission of the journal.
Fig. (2)
Fig. (2)
(A) MTT cell proliferation assay performed on days 1 to 5 after transfection of Kelly, NGP and SK-N-AS cells with either a pre-miR-34a molecule or a negative control oligonucleotide that does not encode for any known miRNA. Cell populations transfected with the negative control oligo had a significantly greater number of metabolically active cells than cells transfected with the pre-miR-34a. (B) Caspase 3/7 assay carried out on Kelly, NGP and SKN-AS cells shows that ectopic up-regulation of miR-34a (diagonal stripe) leads to an increase in caspase activity relative to a negative control oligonuclotide (gray). This figure was originally published by Welch et al [28] in Oncogene and is reproduced here with the permission of the journal.
Fig. (3)
Fig. (3)
MiR34a genetic pathway. The MYCN transcription factor directly up-regulates the transcription of MDM2, which antagonizes the action of the p53 transcription factor. The down-regulation of P53 protein by MDM2 should indirectly cause the down-regulation of miR-34a, which requires p53 for expression. MiR-34a must be down-regulated in neuroblastoma because it directly targets MYCN and other proteins that either promote cell proliferation or retard apoptosis. Mir-34a is also down-regulated by chromosome 1p deletion in some tumors.
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