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ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
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Research Article

EZH2 as a Therapeutic Target in Glioblastoma: A Cellular and Molecular Study

Javier de la Rosa1, Marta Iraburu1, Gabriel Gallo-Oller1, Mehdi H Shahi2, Bárbara Meléndez3, Juan A Rey4, Miguel A Idoate5, and Javier S Castresana1*

1Department of Biochemistry and Genetics, University of Navarra School of Sciences, Pamplona, Spain

2Interdisciplinary Brain Research Centre, Faculty of Medicine, Aligarh Muslim University, Aligarh, India

3Molecular Pathology Research Unit, Virgen de la Salud Hospital, Toledo, Spain

4IdiPaz Research Unit, La Paz University Hospital, Madrid, Spain

5Department of Pathology, University of Navarra Clinic, Pamplona, Spain

Corresponding Author:
Javier S Castresana
Department of Biochemistry and Genetics
University of Navarra School of Sciences, Irunlarrea 1, 31008 Pamplona, Spain
Tel: +34-948-425600\806486
E-mail: [email protected]

Received Date: November 07, 2016; Accepted Date: November 30, 2016; Published Date: December 02, 2016

Citation: de la Rosa J, Iraburu M, Gallo-Oller G, Shahi MH, Meléndez B, et al. (2016) EZH2 as a Therapeutic Target in Glioblastoma: A Cellular and Molecular Study. J Carcinog Mutagen 7:278. doi: 10.4172/2157-2518.1000278

Copyright: © 2016 De la Rosa J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Glioblastoma is the most common malignant brain tumor in adults and it is currently treated with a combination of surgery, radiotherapy and chemotherapy with temozolomide (TMZ). Many patients show resistance to TMZ, which is a challenge in the treatment of this type of brain cancer. New strategies are being tested, like the inhibition of EZH2, a histone methyltransferase which is overexpressed in cancer cells, leading to angiogenesis and metastasis. In this work, the EZH2 inhibitor DZNeP was tested in A172 glioblastoma cells and in A172-TMZ-resistant glioblastoma cells. Inhibition of cell proliferation, adhesion, colony formation, and migration was noted in control and TMZresistant glioblastoma cells after DZNeP treatment. At the level of EZH2 target gene expression, DZNeP decreased EZH2 expression, and increased the expression of its target genes (E-cadherin and TIMP3), which might probably contribute to inhibiting the development of a cancer metastatic phenotype. Finally, DZNeP negatively regulated the TGFβ pathway. In conclusion, we propose that inhibition of EZH2 might be considered as a therapeutic strategy against glioblastoma.

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