Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Urdiciain-Ezpeleta, A. (Alejandro) | - |
dc.creator | Meléndez, B. (Bárbara) | - |
dc.creator | Rey, J.A. (Jorge Alberto) | - |
dc.creator | Idoate, M.A. (Miguel Ángel) | - |
dc.creator | Saez-Castresana, J. (Javier) | - |
dc.date.accessioned | 2023-04-18T06:49:32Z | - |
dc.date.available | 2023-04-18T06:49:32Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Urdiciain-Ezpeleta, A. (Alejandro); Meléndez, B. (Bárbara); Rey, J.A. (Jorge Alberto); et al. "Panobinostat potentiates temozolomide effects and reverses epithelial-mesenchymal transition in glioblastoma cells". Epigenomes. 2 (1), 2018, | es_ES |
dc.identifier.issn | 2075-4655 | - |
dc.identifier.uri | https://hdl.handle.net/10171/65958 | - |
dc.description.abstract | Glioblastoma is the most common form of glioma, as well as the most aggressive. Patients suffering from this disease have a very poor prognosis. Surgery, radiotherapy, and temozolomide are the only approved treatments nowadays. Panobinostat is a pan-inhibitor of histone deacetylases (HDACs) that has been shown to break some pathways which play an important role in cancer development. A global intention of using panobinostat as a therapeutic agent against glioblastoma is beginning to be a reality. We have treated the LN405 glioblastoma cell line with temozolomide, panobinostat, and combined treatment, in order to test apoptosis, colony formation, and a possible molecular reversion of the mesenchymal phenotype of the cells to an epithelial one. Our results show that panobinostat decreased N-cadherin levels in the LN405 glioblastoma cell line while it increased the expression of E-cadherin, which might be associated with a mesenchymal–epithelial transition in glioblastoma cells. Colony formation was reduced, and apoptosis was increased with treatments. Our research highlights the importance of panobinostat as a potential adjuvant therapy to be used with temozolomide to treat glioblastoma and the advantages of the combined treatment versus temozolomide alone, which is currently the first-line treatment used to treat this tumor | es_ES |
dc.description.sponsorship | Financial support for this work was provided by a grant from the Fundación Universidad de Navarra, Pamplona, Spain. A.U. received a predoctoral fellowship from the Asociación de Amigos de la Universidad de Navarra, Pamplona, Spain | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI AG | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.subject | Panobinostat | es_ES |
dc.subject | Temozolomide | es_ES |
dc.subject | Glioblastoma | es_ES |
dc.subject | Epithelial-mesenchymal transition | es_ES |
dc.title | Panobinostat potentiates temozolomide effects and reverses epithelial-mesenchymal transition in glioblastoma cells | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.description.note | This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | es_ES |
dc.identifier.doi | 10.3390/epigenomes2010005 | - |
dadun.citation.number | 1 | es_ES |
dadun.citation.publicationName | Epigenomes | es_ES |
dadun.citation.volume | 2 | es_ES |
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