Potential role of mirnas in the acquisition of chemoresistance in neuroblastoma

Barbara Marengo, Alessandra Pulliero, Maria Valeria Corrias, Riccardo Leardi, Emanuele Farinini, Gilberto Fronza, Paola Menichini, Paola Monti, Lorenzo Monteleone, Giulia Elda Valenti, Andrea Speciale, Patrizia Perri, Francesca Madia, Alberto Izzotti, Cinzia Domenicotti

Research output: Contribution to journalArticlepeer-review

Abstract

Neuroblastoma (NB) accounts for about 8–10% of pediatric cancers, and the main causes of death are the presence of metastases and the acquisition of chemoresistance. Metastatic NB is characterized by MYCN amplification that correlates with changes in the expression of miRNAs, which are small non-coding RNA sequences, playing a crucial role in NB development and chemoresistance. In the present study, miRNA expression was analyzed in two human MYCN-amplified NB cell lines, one sensitive (HTLA-230) and one resistant to Etoposide (ER-HTLA), by microarray and RT-qPCR techniques. These analyses showed that miRNA-15a,-16-1,-19b,-218, and-338 were down-regulated in ER-HTLA cells. In order to validate the presence of this down-regulation in vivo, the expression of these miRNAs was analyzed in primary tumors, metastases, and bone marrow of therapy responder and non-responder pediatric patients. Principal component analysis data showed that the expression of miRNA-19b,-218, and-338 influenced metastases, and that the expression levels of all miRNAs analyzed were higher in therapy responders in respect to non-responders. Collectively, these findings suggest that these miRNAs might be involved in the regulation of the drug response, and could be employed for therapeutic purposes.

Original languageEnglish
Article number107
Pages (from-to)1-17
Number of pages17
JournalJournal of Personalized Medicine
Volume11
Issue number2
DOIs
Publication statusPublished - Feb 2021

Keywords

  • Chemoresistance
  • Metastases
  • MiRNA
  • MYCN amplification
  • Neuroblastoma

ASJC Scopus subject areas

  • Medicine (miscellaneous)

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