miRNA expression profile of bone marrow resident cells from children with neuroblastoma is not significantly different from that of healthy children
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Sara Stigliani1,*, Fabio Morandi2,5,*, Luca Persico3, Corrado Lagazio3, Giovanni Erminio4, Paola Scaruffi1 and Maria Valeria Corrias2
1Physiopathology of Human Reproduction, Ospedale Policlinico San Martino, Genoa, Italy
2Experimental Therapy in Oncology, IRCCS Istituto Giannina Gaslini, Genoa, Italy
3Department of Economy, University of Genoa, Genoa, Italy
4Epidemiology, Biostatistics and Committees, IRCCS Istituto Giannina Gaslini, Genoa, Italy
5Present address: Stem Cell Laboratory and Cell Therapy Center, IRCCS Istituto Giannina Gaslini, Genoa, Italy
*These authors contributed equally to this work
Maria Valeria Corrias, email: [email protected]
Keywords: miRNA; neuroblastoma; bone marrow; mitochondria; gene expression
Received: August 29, 2017 Accepted: March 02, 2018 Published: April 10, 2018
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.
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