MicroRNAs-Proteomic Networks Characterizing Human Medulloblastoma-SLCs. (6th January 2016)

• Record Type: Journal Article
• Authors: Catanzaro, Giuseppina; Besharat, Zein Mersini; Garg, Neha; Ronci, Maurizio; Pieroni, Luisa; Miele, Evelina; Mastronuzzi, Angela; Carai, Andrea; Alfano, Vincenzo; Po, Agnese; Screpanti, Isabella; Locatelli, Franco; Urbani, Andrea; Ferretti, Elisabetta
• Other Names: Rangel Maria C. Academic Editor.
• Is Part Of: Stem cells international. Volume 2016(2016)
• Publication Date: 2016-01-06
• Subjects: Stem Cells -- Periodicals; Stem Cells -- Therapeutic use -- Periodicals; Stem Cells -- Transplantation -- Periodicals; 616.0277405
• DOI: 10.1155/2016/2683042
• Languages: English
• ISSNs: 1687-966X

Abstract

Abstract : Medulloblastoma (MB) is the most common malignant brain tumor of pediatric age and is characterized by cells expressing stem, astroglial, and neuronal markers. Among them, stem-like cells (hMB-SLCs) represent a fraction of the tumor cell population with the potential of self-renewal and proliferation and have been associated with tumor poor prognosis. In this context, microRNAs have been described as playing a pivotal role in stem cells differentiation. In our paper, we analyze microRNAs profile and genes expression of hMB-SLCs before and after Retinoic Acid- (RA-) induced differentiation. We aimed to identify pivotal players of specific pathways sustaining stemness and/or tumor development and progression and integrate the results of our recent proteomic study. Our results uncovered 22 differentially expressed microRNAs that were used as input together with deregulated genes and proteins in the Genomatix Pathway System (GePS) analysis revealing 3 subnetworks that could be interestingly involved in the maintenance of hMB-SLCs proliferation. Taken together, our findings highlight microRNAs, genes, and proteins that are significantly modulated in hMB-SLCs with respect to their RA-differentiated counterparts and could open new perspectives for prognostic and therapeutic intervention on MB.