Erausquin, E. (Elena)

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    Silencing of histone deacetylase 6 decreases cellular malignancy and contributes to primary cilium restoration, epithelial-to-mesenchymal transition reversion, and autophagy inhibition in glioblastoma cell lines
    (MDPI AG, 2021) Lanciego, J.L. (José Luis); Urdiciain-Ezpeleta, A. (Alejandro); Saez-Castresana, J. (Javier); Rey, J.A. (Juan A.); Erausquin, E. (Elena); Zelaya, M.V. (María Victoria); Zazpe, I. (Idoya); Idoate, M.A. (Miguel Ángel); Riobo-Del-Galdo, N.A. (Natalia A.); Meléndez, B. (Bárbara)
    Glioblastoma multiforme, the most common type of malignant brain tumor as well as the most aggressive one, lacks an effective therapy. Glioblastoma presents overexpression of mesenchymal markers Snail, Slug, and N-Cadherin and of the autophagic marker p62. Glioblastoma cell lines also present increased autophagy, overexpression of mesenchymal markers, Shh pathway activation, and lack of primary cilia. In this study, we aimed to evaluate the role of HDAC6 in the pathogenesis of glioblastoma, as HDAC6 is the most overexpressed of all HDACs isoforms in this tumor. We treated glioblastoma cell lines with siHDAC6. HDAC6 silencing inhibited proliferation, migration, and clonogenicity of glioblastoma cell lines. They also reversed the mesenchymal phenotype, decreased autophagy, inhibited Shh pathway, and recovered the expression of primary cilia in glioblastoma cell lines. These results demonstrate that HDAC6 might be a good target for glioblastoma treatment.
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    Tubastatin A, an inhibitor of HDAC6, enhances temozolomide‐induced apoptosis and reverses the malignant phenotype of glioblastoma cells
    (Spandidos publications, 2019) Urdiciain-Ezpeleta, A. (Alejandro); Saez-Castresana, J. (Javier); Rey, J.A. (Juan A.); Erausquin, E. (Elena); Idoate, M.A. (Miguel Ángel); Meléndez, B. (Bárbara)
    Glioblastoma or grade IV astrocytoma is the most common and lethal form of glioma. Current glioblastoma treatment strategies use surgery followed by chemotherapy with temozolomide. Despite this, numerous glioblastoma cases develop resistance to temozolomide treatments, resulting in a poor prognosis for the patients. Novel approaches are being investigated, including the inhibition of histone deacetylase 6 (HDAC6), an enzyme that deacetylates α-tubulin, and whose overexpression in glioblastoma is associated with the loss of primary cilia. The aim of the present study was to treat glioblastoma cells with a selective HDAC6 inhibitor, tubastatin A, to determine if the malignant phenotype may be reverted. The results demonstrated a notable increase in acetylated α-tubulin levels in treated cells, which associated with downregulation of the sonic hedgehog pathway, and may hypothetically promote ciliogenesis in those cells. Treatment with tubastatin A also reduced glioblastoma clonogenicity and migration capacities, and accelerated temozolomide-induced apoptosis. Finally, HDAC6 inhibition decreased the expression of mesenchymal markers, contributing to reverse epithelial-mesenchymal transition in glioblastoma cells.