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Bromodomain and Extraterminal Domain (BET) Protein Inhibition Hinders Glioblastoma Progression by Inducing Autophagy-Dependent Differentiation.
Colardo, Mayra; Gargano, Deborah; Russo, Miriam; Petraroia, Michele; Pensabene, Daniele; D'Alessandro, Giuseppina; Santoro, Antonio; Limatola, Cristina; Segatto, Marco; Di Bartolomeo, Sabrina.
Afiliación
  • Colardo M; Department of Biosciences and Territory, University of Molise, 86090 Pesche, Italy.
  • Gargano D; Department of Biosciences and Territory, University of Molise, 86090 Pesche, Italy.
  • Russo M; Department of Biosciences and Territory, University of Molise, 86090 Pesche, Italy.
  • Petraroia M; Department of Biosciences and Territory, University of Molise, 86090 Pesche, Italy.
  • Pensabene D; Department of Science, University Roma Tre, 00146 Rome, Italy.
  • D'Alessandro G; Department of Physiology and Pharmacology, Laboratory Affiliated to Istituto Pasteur Italia, Sapienza University of Rome, 00185 Rome, Italy.
  • Santoro A; Neuromed IRCCS, Via Atinense, 86077 Pozzilli, Italy.
  • Limatola C; Department of Human Neuroscience, Sapienza University of Rome, 00185 Rome, Italy.
  • Segatto M; Department of Physiology and Pharmacology, Laboratory Affiliated to Istituto Pasteur Italia, Sapienza University of Rome, 00185 Rome, Italy.
  • Di Bartolomeo S; Neuromed IRCCS, Via Atinense, 86077 Pozzilli, Italy.
Int J Mol Sci ; 24(8)2023 Apr 10.
Article en En | MEDLINE | ID: mdl-37108181
Glioblastoma multiforme (GBM) is the most common and aggressive type of malignant primary brain tumor, and it is characterized by a high recurrence incidence and poor prognosis due to the presence of a highly heterogeneous mass of stem cells with self-renewal capacity and stemness maintenance ability. In recent years, the epigenetic landscape of GBM has been explored and many epigenetic alterations have been investigated. Among the investigated epigenetic abnormalities, the bromodomain and extra-terminal domain (BET) chromatin readers have been found to be significantly overexpressed in GBM. In this work, we investigated the effects of BET protein inhibition on GBM cell reprogramming. We found that the pan-BET pharmacological inhibitor JQ1 was able to promote a differentiation program in GBM cells, thus impairing cell proliferation and enhancing the toxicity of the drug Temozolomide (TMZ). Notably, the pro-differentiation capability of JQ1 was prevented in autophagy-defective models, suggesting that autophagy activation is necessary for BET protein activity in regulating glioma cell fate. Given the growing interest in epigenetic therapy, our results further support the possibility of introducing a BET-based approach in GBM clinical management.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glioblastoma Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Glioblastoma Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza