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NRF2 drives glioma malignancy through transcriptional activation of an important oncogenic mechanism

AutorLastra, Diego; Pajares, María A. ; Gargini, Ricardo ; Cuadrado, Antonio ; Escoll, Maribel
Fecha de publicación2017
CitaciónFEBS3+ (2017)
XL SEBBM Congress (2017)
ResumenGliomas are nervous system solid tumors with poor prognosis and hard treatment, since they present cancer stem cells (CSCs), a subpopulation of tumor cells responsible of tumor initiation, treatment resistance, metastasis and recurrence, producing highly aggressive phenotypes. The transcription factor NRF2 (nuclear factor (erythroid-derived 2)-like 2), a master regulator of homeostasis, has been widely described as a tumor growth promoter, implicated in tumor survival and drug resistance. However, despite it has also been implied in CSCs’ metabolism, its importance remains unclear. Our study has identified for the first time how NRF2 is able of promoting CSCs maintenance and survival stimulating the transcription of an important oncogenic effector through novel identified ARE elements (Antioxidant Response Elements, functional NRF2-binding sites). In addition, we have identified a clear correlation between levels of expression of NRF2 and the prognosis of glioma patients. Overall, our studies show a new oncogenic mechanism through which NRF2 produces tumorogenesis and CSCs maintenance. Consequently, we propose NRF2 as a new therapeutic target and prognosis marker in gliomas.
DescripciónResumen del póster presentado al 1st Joint Meeting of the French-Portuguese-Spanish Biochemical and Molecular Biology Societies y al XL Spanish Society of Biochemistry and Molecular Biology (SEBBM) Congress, celebrado en Barcelona (España) del 23 al 26 de octubre de 2017.
URIhttp://hdl.handle.net/10261/163921
Aparece en las colecciones: (IIBM) Comunicaciones congresos
(CBM) Comunicaciones congresos
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