Role of redox status in development of glioblastoma

Glioblastoma (GBM) is a highly aggressive neoplasia, prognosis remains dismal and current therapy is mostly palliative. There are no known risk factors associated with gliomagenesis; however, it is well established that chronic inflammation in brain tissue induces oxidative stress in astrocytes and...

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Main Authors: Aleli eSalazar-Ramiro, Daniela eRamírez-Ortega, Norma Y. Hérnandez-Pedro, Dinora Fabiola eGonzalez Esquivel, Julio eSotelo, Verónica ePérez de la Cruz, Benjamin ePineda
Format: Article
Language:English
Published: Frontiers Media S.A. 2016-04-01
Series:Frontiers in Immunology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00156/full
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author Aleli eSalazar-Ramiro
Daniela eRamírez-Ortega
Norma Y. Hérnandez-Pedro
Dinora Fabiola eGonzalez Esquivel
Julio eSotelo
Verónica ePérez de la Cruz
Benjamin ePineda
author_facet Aleli eSalazar-Ramiro
Daniela eRamírez-Ortega
Norma Y. Hérnandez-Pedro
Dinora Fabiola eGonzalez Esquivel
Julio eSotelo
Verónica ePérez de la Cruz
Benjamin ePineda
author_sort Aleli eSalazar-Ramiro
collection DOAJ
description Glioblastoma (GBM) is a highly aggressive neoplasia, prognosis remains dismal and current therapy is mostly palliative. There are no known risk factors associated with gliomagenesis; however, it is well established that chronic inflammation in brain tissue induces oxidative stress in astrocytes and microglia. High quantities of reactive species of oxygen into the cells can react with several macromolecules, including chromosomal and mitochondrial DNA, leading to damage and malfunction of DNA repair enzymes. These changes bring genetic instability and abnormal metabolic processes favoring oxidative environment and increase rate of cell proliferation. In GBM, a high metabolic rate and increased basal levels of ROS play an important role as chemical mediators in the regulation of signal transduction, protecting malignant cells from apoptosis, thus creating an immunosuppressive environment. New redox therapeutics could reduce oxidative stress preventing cellular damage and high mutation rate accompanied by chromosomal instability, reducing the immunosuppressive environment. In addition, therapies directed to modulate redox rate reduce resistance and moderate the high rate of cell proliferation, favoring apoptosis of tumoral cells. This review describes the redox status in GBM and how this imbalance could promote gliomagenesis through genomic and mitochondrial DNA damage, inducing the pro-oxidant and pro-inflammatory environment involved in tumor cell proliferation, resistance and immune scape. In addition, are described some therapeutic agents that modulate redox status and might be advantageous in therapy against GBM.
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spelling doaj.art-825f2c6def494c348f29312d06ff19dc2022-12-22T01:50:42ZengFrontiers Media S.A.Frontiers in Immunology1664-32242016-04-01710.3389/fimmu.2016.00156185411Role of redox status in development of glioblastomaAleli eSalazar-Ramiro0Daniela eRamírez-Ortega1Norma Y. Hérnandez-Pedro2Dinora Fabiola eGonzalez Esquivel3Julio eSotelo4Verónica ePérez de la Cruz5Benjamin ePineda6National Institute of Neurology and Neurosurgery (INNN)National Institute of Neurology and Neurosurgery (INNN)National Cancer Institute (INCAN)National Institute of Neurology and Neurosurgery (INNN)National Institute of Neurology and Neurosurgery (INNN)National Institute of Neurology and Neurosurgery (INNN)National Institute of Neurology and Neurosurgery (INNN)Glioblastoma (GBM) is a highly aggressive neoplasia, prognosis remains dismal and current therapy is mostly palliative. There are no known risk factors associated with gliomagenesis; however, it is well established that chronic inflammation in brain tissue induces oxidative stress in astrocytes and microglia. High quantities of reactive species of oxygen into the cells can react with several macromolecules, including chromosomal and mitochondrial DNA, leading to damage and malfunction of DNA repair enzymes. These changes bring genetic instability and abnormal metabolic processes favoring oxidative environment and increase rate of cell proliferation. In GBM, a high metabolic rate and increased basal levels of ROS play an important role as chemical mediators in the regulation of signal transduction, protecting malignant cells from apoptosis, thus creating an immunosuppressive environment. New redox therapeutics could reduce oxidative stress preventing cellular damage and high mutation rate accompanied by chromosomal instability, reducing the immunosuppressive environment. In addition, therapies directed to modulate redox rate reduce resistance and moderate the high rate of cell proliferation, favoring apoptosis of tumoral cells. This review describes the redox status in GBM and how this imbalance could promote gliomagenesis through genomic and mitochondrial DNA damage, inducing the pro-oxidant and pro-inflammatory environment involved in tumor cell proliferation, resistance and immune scape. In addition, are described some therapeutic agents that modulate redox status and might be advantageous in therapy against GBM.http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00156/fullDNA DamageGlioblastomaTumor Microenvironmentredox statusgliomagenesis
spellingShingle Aleli eSalazar-Ramiro
Daniela eRamírez-Ortega
Norma Y. Hérnandez-Pedro
Dinora Fabiola eGonzalez Esquivel
Julio eSotelo
Verónica ePérez de la Cruz
Benjamin ePineda
Role of redox status in development of glioblastoma
Frontiers in Immunology
DNA Damage
Glioblastoma
Tumor Microenvironment
redox status
gliomagenesis
title Role of redox status in development of glioblastoma
title_full Role of redox status in development of glioblastoma
title_fullStr Role of redox status in development of glioblastoma
title_full_unstemmed Role of redox status in development of glioblastoma
title_short Role of redox status in development of glioblastoma
title_sort role of redox status in development of glioblastoma
topic DNA Damage
Glioblastoma
Tumor Microenvironment
redox status
gliomagenesis
url http://journal.frontiersin.org/Journal/10.3389/fimmu.2016.00156/full
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AT danielaeramirezortega roleofredoxstatusindevelopmentofglioblastoma
AT normayhernandezpedro roleofredoxstatusindevelopmentofglioblastoma
AT dinorafabiolaegonzalezesquivel roleofredoxstatusindevelopmentofglioblastoma
AT julioesotelo roleofredoxstatusindevelopmentofglioblastoma
AT veronicaeperezdelacruz roleofredoxstatusindevelopmentofglioblastoma
AT benjaminepineda roleofredoxstatusindevelopmentofglioblastoma