Panobinostat Potentiates Temozolomide Effects and Reverses Epithelial–Mesenchymal Transition in Glioblastoma Cells

• Main Authors: Alejandro Urdiciain, Bárbara Meléndez, Juan A. Rey, Miguel A. Idoate, Javier S. Castresana
• Format: Article
• Language: English
• Published: MDPI AG 2018-02-01
• Series: Epigenomes
• Subjects: panobinostat; temozolomide; glioblastoma; epithelial-mesenchymal transition
• Online Access: http://www.mdpi.com/2075-4655/2/1/5

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.