Research Papers:
The histone methyltransferase EZH2 as a druggable target in SHH medulloblastoma cancer stem cells
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Abstract
Evelina Miele1,10,*, Sergio Valente2,*, Vincenzo Alfano3, Marianna Silvano3, Paolo Mellini2, Diana Borovika4, Biagina Marrocco2, Agnese Po5, Zein Mersini Besharat5, Giuseppina Catanzaro3, Giuseppe Battaglia6, Luana Abballe3, Clemens Zwergel2, Giulia Stazi2, Ciro Milite7, Sabrina Castellano7,8, Marco Tafani3, Peteris Trapencieris4, Antonello Mai2,9 and Elisabetta Ferretti3,6
1Center for Life NanoScience@Sapienza, Istituto Italiano di Tecnologia, Rome 00161, Italy
2Department of Chemistry and Technologies of Drugs, Sapienza University of Rome, Rome 00185, Italy
3Department of Experimental Medicine, Sapienza University of Rome, Rome 00161, Italy
4Latvian Institute of Organic Synthesis, Riga LV-1006, Latvia
5Department of Molecular Medicine, Sapienza University of Rome, Rome 00161, Italy
6Neuromed Institute, Località Camerelle, Pozzilli 86077, Italy
7Department of Pharmacy, University of Salerno, Fisciano 84084, Italy
8Department of Medicine and Surgery, University of Salerno, Baronissi 84084, Italy
9Pasteur Institute, Cenci-Bolognetti Foundation, Sapienza University of Rome, Rome 00185, Italy
10Current address: Department of Hematology/Oncology and Stem Cell Transplantation, Bambino Gesù, 28 Children’s Hospital, IRCCS, Rome 00165, Italy
*These authors have contributed equally to this work
Correspondence to:
Elisabetta Ferretti, email: [email protected]
Antonello Mai, email: [email protected]
Keywords: histone methyltransferase, EZH2 inhibitors, hedgehog pathway, medulloblastoma stem-like cells, self-renewal
Received: November 18, 2016 Accepted: June 20, 2017 Published: August 02, 2017
ABSTRACT
The histone methyltransferase EZH2 plays a role in maintenance of the stem component of cancer, and its overexpression and/or mutation typically drives tumor aggressiveness, drug resistance and patients’ poor prognosis. In this study, we use mouse and human medulloblastoma stem-like cells belonging to the Sonic Hedgehog subgroup (SHH MB-SLCs) and demonstrate that genetic suppression of EZH2 reduces the level of its histone mark H3K27me3 and lowers proliferation and self-renewal. We designed an EZH2 inhibitor (EZH2i) as a simplified analog of EPZ005687 and GSK2816126, MC3629, and we tested its biological activity in SHH MB-SLCs. Pharmacological inhibition of EZH2 impairs SHH MB cells proliferation and self-renewal, and induces apoptosis in vitro. Finally, we generated xenograft MB-SLCs orthotopic tumors in nude mice to test MC3629 in vivo. In treated mice, we observed impairment of tumor growth, together with induction of apoptosis and reduction of proliferation and stemness.
Overall, these findings describe EZH2 as a druggable target in MB and provide insight into the biological activity of MC3629 as an EZH2i.
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