Abstract
The miRNA expression profiles of bone marrow resident cells from children with neuroblastoma were compared to that of healthy children. No significant difference was found between localized and metastatic neuroblastoma, or between children with neuroblastoma and healthy children. By considering the fold change we identified six miRNAs over-expressed by more than 150 fold in neuroblastoma. Validation confirmed miR-221 over-expression in BM resident cells from children with neuroblastoma, regardless of localized or metastatic disease.MiR-221 over-expression was unlikely derived from neuroblastoma primary tumors or from bone marrow-infiltrating metastatic cells, since neuroblastoma cells expressed lower or similar amount of miR-221 than BM cells, respectively.To get insight on the genes potentially regulated by miR-221 we merged the list of miR-221 potential targets with the genes under-expressed by BM resident cells from children with neuroblastoma, as compared with healthy children. In silico analysis demonstrated that none of the miR-221 target genes belonged to heme biosynthetic processes found altered in children with neuroblastoma, whereas two genes associated with mitochondria. However, the encoded proteins were not under-expressed in children with neuroblastoma, making unlikely that altered erythrocyte maturation in children with neuroblastoma was mediated by miR-221.In conclusion, miRNA expression profiles of BM resident cells from children with localized and metastatic neuroblastoma were similar to that of BM resident cells from healthy children. Moreover, miRNAs expressed by neuroblastoma primary tumors or by BM-infiltrating NB cells do not appear to be involved in mediating the functional defect of erythrocyte maturation recently observed in children with neuroblastoma.
Highlights
MiRNAs are 20–22 nucleotide-long non coding RNAs that, following binding to complementary sequences in the 3′ UTR of an mRNA, repress translation or induce mRNA degradation
Given the pivotal role of miRNAs in regulating gene expression, here we investigated whether the decreased expression of these genes was regulated by specific miRNA(s) over-expressed by bone marrow (BM) resident cells of children with NB, as compared with healthy children
Twelve BM resident cell samples from healthy children, twelve from children with localized NB and twelve from children with metastatic NB were identified in our RNA bio bank (Table 1)
Summary
MiRNAs are 20–22 nucleotide-long non coding RNAs that, following binding to complementary sequences in the 3′ UTR of an mRNA, repress translation or induce mRNA degradation. MiRNAs are considered major regulators of gene expression in both normal and neoplastic cells [1]. Since they can be found in plasma, either free or inside tumor-derived vesicles that can fuse to cells of different lineages, miRNAs can regulate gene expression at distance [2,3,4]. Metastatic disease mainly involves the bone marrow (BM), and presence of BM-infiltrating NB cells is the main negative prognostic factor [6]. Prognostic miRNA expression profiles of human NB primary tumors have been defined [11,12,13], and public datasets of miRNA expression levels in specific subsets of human NB primary tumors are available (GSE86889, GSE21713, GSE16444) [14,15,16]
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