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 tumo