ArticleRedox biology2020
Transcription factor NRF2 uses the Hippo pathway effector TAZ to induce tumorigenesis in glioblastomas.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Lymphatic Metastasis of Esophageal Squamous Cell Carcinoma: The Role of NRF2 and Therapeutic Strategies.Cancers · 2025Review
- TAZ/NRF2 positive feedback loop contributes to proliferation in bladder cancer through antagonistic ferroptosis.Cell death discovery · 2025Article
- Knockdown of BAP31 Suppresses Tumorigenesis and Stemness in Breast Cancer Cells via the Hippo Pathway.International journal of molecular sciences · 2025Article
- TAZ deficiency impairs the autophagy-lysosomal pathway through NRF2 dysregulation and lysosomal dysfunction.International journal of biological sciences · 2024Article
- Emerging Role of NRF2 Signaling in Cancer Stem Cell Phenotype.Molecules and cells · 2023Review
- Transcriptome Changes in Glioma Cells Cultivated under Conditions of Neurosphere Formation.Cells · 2022Article
- Adaptive Changes Allow Targeting of Ferroptosis for Glioma Treatment.Cellular and molecular neurobiology · 2022Review
- The Role of NRF2/KEAP1 Pathway in Glioblastoma: Pharmacological Implications.Medical oncology (Northwood, London, England) · 2022Review
- Transcription Factor NRF2 Participates in Cell Cycle Progression at the Level of G1/S and Mitotic Checkpoints.Antioxidants (Basel, Switzerland) · 2022Article
- MicroRNA-147a Targets SLC40A1 to Induce Ferroptosis in Human Glioblastoma.Analytical cellular pathology (Amsterdam) · 2022Article
- Hippo Pathway in Regulating Drug Resistance of Glioblastoma.International journal of molecular sciences · 2021Review
- LncRNA MIR4435-2HG functions as a ceRNA against miR-125a-5p and promotes neuroglioma development by upregulating TAZ.Journal of clinical laboratory analysis · 2021Article
- α-Synuclein Induces the GSK-3-Mediated Phosphorylation and Degradation of NURR1 and Loss of Dopaminergic Hallmarks.Molecular neurobiology · 2021Article
- Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021Review
- Biomaterials Regulate Mechanosensors YAP/TAZ in Stem Cell Growth and Differentiation.Tissue engineering and regenerative medicine · 2021Review
- Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery.Antioxidants (Basel, Switzerland) · 2021Review
- Hippo Signaling Pathway in Gliomas.Cells · 2021Review
- Interplay between Mitochondrial Metabolism and Cellular Redox State Dictates Cancer Cell Survival.Oxidative medicine and cellular longevity · 2021Review
- Bevacizumab-Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor NRF2 orchestrates a cellular defense against oxidative stress and, so far, has been involved in tumor progression by providing a metabolic adaptation to tumorigenic demands and resistance to chemotherapeutics. In this study, we discover that NRF2 also propels tumorigenesis in gliomas and glioblastomas by inducing the expression of the transcriptional co-activator TAZ, a protein of the Hippo signaling pathway that promotes tumor growth. The expression of the genes encoding NRF2 (NFE2L2) and TAZ (WWTR1) showed a positive correlation in 721 gliomas from The Cancer Genome Atlas database. Moreover, NRF2 and TAZ protein levels also correlated in immunohistochemical tissue arrays of glioblastomas. Genetic knock-down of NRF2 decreased, while NRF2 overexpression or chemical activation with sulforaphane, increased TAZ transcript and protein levels. Mechanistically, we identified several NRF2-regulated functional enhancers in the regulatory region of WWTR1. The relevance of the new NRF2/TAZ axis in tumorigenesis was demonstrated in subcutaneous and intracranial grafts. Thus, intracranial inoculation of NRF2-depleted glioma stem cells did not develop tumors as determined by magnetic resonance imaging. Forced TAZ overexpression partly rescued both stem cell growth in neurospheres and tumorigenicity. Hence, NRF2 not only enables tumor cells to be competent to proliferate but it also propels tumorigenesis by activating the TAZ-mediated Hippo transcriptional program.
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