Temozolomide Resistance in Glioblastoma by NRF2: Protecting the Evil

The transcription factor NRF2 is constitutively active in glioblastoma, a highly aggressive brain tumor subtype with poor prognosis. Temozolomide (TMZ) is the primary chemotherapeutic agent for this type of tumor treatment, but resistance to this drug is often observed. This review highlights the re...

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Published inBiomedicines Vol. 11; no. 4; p. 1081
Main Authors Almeida Lima, Karoline, Osawa, Isabeli Yumi Araújo, Ramalho, Maria Carolina Clares, de Souza, Izadora, Guedes, Camila Banca, Souza Filho, Cláudio Henrique Dahne de, Monteiro, Linda Karolynne Seregni, Latancia, Marcela Teatin, Rocha, Clarissa Ribeiro Reily
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.04.2023
MDPI
Subjects
1-Phosphatidylinositol 3-kinase
AKT protein
Antimitotic agents
Antineoplastic agents
Antioxidants
Apoptosis
Autophagy
Brain cancer
Brain tumors
Cancer therapies
Cell cycle
Chemoresistance
Chemotherapy
Detoxification
DNA damage
DNA methylation
DNA repair
Dosage and administration
Glioblastoma
Kinases
Medical prognosis
MicroRNAs
Mutation
NRF2
Oxidative stress
Patient outcomes
Physiology
Proteins
Review
Temozolomide
Therapeutic targets
Transcription factors
United States
temozolomide
NRF2
glioblastoma
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Abstract The transcription factor NRF2 is constitutively active in glioblastoma, a highly aggressive brain tumor subtype with poor prognosis. Temozolomide (TMZ) is the primary chemotherapeutic agent for this type of tumor treatment, but resistance to this drug is often observed. This review highlights the research that is demonstrating how NRF2 hyperactivation creates an environment that favors the survival of malignant cells and protects against oxidative stress and TMZ. Mechanistically, NRF2 increases drug detoxification, autophagy, DNA repair, and decreases drug accumulation and apoptotic signaling. Our review also presents potential strategies for targeting NRF2 as an adjuvant therapy to overcome TMZ chemoresistance in glioblastoma. Specific molecular pathways, including MAPKs, GSK3β, βTRCP, PI3K, AKT, and GBP, that modulate NRF2 expression leading to TMZ resistance are discussed, along with the importance of identifying NRF2 modulators to reverse TMZ resistance and develop new therapeutic targets. Despite the significant progress in understanding the role of NRF2 in GBM, there are still unanswered questions regarding its regulation and downstream effects. Future research should focus on elucidating the precise mechanisms by which NRF2 mediates resistance to TMZ, and identifying potential novel targets for therapeutic intervention.
AbstractList The transcription factor NRF2 is constitutively active in glioblastoma, a highly aggressive brain tumor subtype with poor prognosis. Temozolomide (TMZ) is the primary chemotherapeutic agent for this type of tumor treatment, but resistance to this drug is often observed. This review highlights the research that is demonstrating how NRF2 hyperactivation creates an environment that favors the survival of malignant cells and protects against oxidative stress and TMZ. Mechanistically, NRF2 increases drug detoxification, autophagy, DNA repair, and decreases drug accumulation and apoptotic signaling. Our review also presents potential strategies for targeting NRF2 as an adjuvant therapy to overcome TMZ chemoresistance in glioblastoma. Specific molecular pathways, including MAPKs, GSK3β, βTRCP, PI3K, AKT, and GBP, that modulate NRF2 expression leading to TMZ resistance are discussed, along with the importance of identifying NRF2 modulators to reverse TMZ resistance and develop new therapeutic targets. Despite the significant progress in understanding the role of NRF2 in GBM, there are still unanswered questions regarding its regulation and downstream effects. Future research should focus on elucidating the precise mechanisms by which NRF2 mediates resistance to TMZ, and identifying potential novel targets for therapeutic intervention.
Audience Academic
Author Almeida Lima, Karoline
Ramalho, Maria Carolina Clares
Guedes, Camila Banca
Rocha, Clarissa Ribeiro Reily
de Souza, Izadora
Monteiro, Linda Karolynne Seregni
Osawa, Isabeli Yumi Araújo
Souza Filho, Cláudio Henrique Dahne de
Latancia, Marcela Teatin
AuthorAffiliation 2 Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA
1 Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil; karoline.almeida@unifesp.br (K.A.L.)
AuthorAffiliation_xml – name: 1 Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil; karoline.almeida@unifesp.br (K.A.L.)
– name: 2 Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA
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  surname: Almeida Lima
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  givenname: Cláudio Henrique Dahne de
  surname: Souza Filho
  fullname: Souza Filho, Cláudio Henrique Dahne de
  organization: Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil
– sequence: 7
  givenname: Linda Karolynne Seregni
  orcidid: 0000-0003-2275-5378
  surname: Monteiro
  fullname: Monteiro, Linda Karolynne Seregni
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  orcidid: 0000-0002-3743-7105
  surname: Latancia
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  givenname: Clarissa Ribeiro Reily
  orcidid: 0000-0001-9634-4307
  surname: Rocha
  fullname: Rocha, Clarissa Ribeiro Reily
  organization: Department of Clinical and Experimental Oncology, Federal University of Sao Paulo (UNIFESP), Sao Paulo 04037-003, Brazil
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37189700$$D View this record in MEDLINE/PubMed
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Keywords temozolomide
NRF2
glioblastoma
Language English
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Snippet The transcription factor NRF2 is constitutively active in glioblastoma, a highly aggressive brain tumor subtype with poor prognosis. Temozolomide (TMZ) is the...
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StartPage 1081
SubjectTerms 1-Phosphatidylinositol 3-kinase
AKT protein
Antimitotic agents
Antineoplastic agents
Antioxidants
Apoptosis
Autophagy
Brain cancer
Brain tumors
Cancer therapies
Cell cycle
Chemoresistance
Chemotherapy
Detoxification
DNA damage
DNA methylation
DNA repair
Dosage and administration
Glioblastoma
Kinases
Medical prognosis
MicroRNAs
Mutation
NRF2
Oxidative stress
Patient outcomes
Physiology
Proteins
Review
Temozolomide
Therapeutic targets
Transcription factors
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Title Temozolomide Resistance in Glioblastoma by NRF2: Protecting the Evil
URI https://www.ncbi.nlm.nih.gov/pubmed/37189700
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https://pubmed.ncbi.nlm.nih.gov/PMC10136186
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Volume 11
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