Περίληψη:
Gliomas portray a large and heterogeneous group of CNS tumors, encompassing a wide range of low-to high-grade tumors, as defined by histological and molecular characteristics. The identification of signature mutations and other molecular abnormalities has largely impacted tumor classification, diagnosis, and therapy. Transcription factors (TFs) are master regulators of gene expression programs, which ultimately shape cell fate and homeostasis. A variety of TFs have been detected to be aberrantly expressed in brain tumors, being highly implicated in critical pathological aspects and progression of gliomas. Herein, we describe a selection of oncogenic (GLI-1/2/3, E2F1–8, STAT3, and HIF-1/2) and tumor suppressor (NFI-A/B, TBXT, MYT1, and MYT1L) TFs that are deregulated in gliomas and are subsequently associated with tumor development, progression, and migratory potential. We further discuss the current targeting options against these TFs, including chemical (Bortezomib) and natural (Plumbagin) compounds, small molecules, and inhibitors, and address their potential implications in glioma therapy. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.
Συγγραφείς:
Giannopoulou, A.-I.
Kanakoglou, D.S.
Piperi, C.
Λέξεις-κλειδιά:
brain tumor; genetics; glioma; human; metabolism; mutation; oncogene; tumor suppressor gene, Brain Neoplasms; Genes, Tumor Suppressor; Glioma; Humans; Mutation; Oncogenes
