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The Dual Roles of NRF2 in Cancer
Open accessAbstract
NRF2 has been traditionally considered as a tumor suppressor because its cytoprotective functions are deemed to be the main cellular defense mechanism against exogenous and endogenous insults, including xenobiotics and oxidative stress. However, several recent studies demonstrate that hyperactivation of the NRF2 pathway creates an environment that favors the survival of normal as well as malignant cells, protecting them against oxidative stress, chemotherapeutic agents, and radiotherapy. In a rapidly advancing field, this review summarizes some of the known mechanisms by which NRF2 can exert its oncogenic functions, and describes the current status of NRF2 inhibitors, providing a clear rationale for the consideration of NRF2 as a powerful putative therapeutic target in cancer treatment.
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“NRF2 is mutationally activated in 10–30% of different solid tumors including liver, lung, stomach, colon and other cancers and mutations typically disrupt the interaction between NRF2 and its E3 ligase KEAP1 (Kelch Like ECH Associated Protein 1) directly or by impeding KEAP1 co-factors CUL3 (Cullin 3) and CAND1 (Cullin Associated and Neddylation Dissociated 1) [2,5,6,7,8].”
From NRF2 Activation Confers Resistance to eIF4A Inhibitors in Cancer Therapy (2021) · cites this paper as [8]
In the citing paper
“NRF2 is mutationally activated in 10–30% of different solid tumors including liver, lung, stomach, colon and other cancers and mutations typically disrupt the interaction between NRF2 and its E3 ligase KEAP1 (Kelch Like ECH Associated Protein 1) directly or by impeding KEAP1 co-factors CUL3 (Cullin 3) and CAND1 (Cullin Associated and Neddylation Dissociated 1) [2,5,6,7,8].”
From NRF2 Activation Confers Resistance to eIF4A Inhibitors in Cancer Therapy (2021) · cites this paper as [8]
In the citing paper
“In this regard, mutations to NRF2 and its regulator KEAP1 have been found in cancer cells, supporting the supposition that antioxidant genes are pivotal in tumor progression59–62.”
From ROS in cancer therapy: the bright side of the moon (2020) · cites this paper as [61]
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Metadata
- Authors
- Menegon, S., Columbano, A., & Giordano, S.
- Affiliations
- Candiolo Cancer Institute (IT)
- University of Cagliari (IT)
- Corresponding author
- Menegon, Silvia
- Columbano, Amedeo
- Giordano, Silvia
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 22
- Issue
- 7
- Pages
- 578-593
- ISSN
- 1471-4914 (ISSN-L)
- OpenAlex
- W2417535489
- Cited by
- 633
- References
- 114
- Citations by year
- 2026: 28 · 2025: 43 · 2024: 64 · 2023: 60 · 2022: 74 · 2021: 75 · 2020: 69 · 2019: 72 · 2018: 73 · 2017: 57 · 2016: 16
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-nd
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, cc-by-nc-nd)
- UNICA IRIS Institutional Research Information System (University of Cagliari) (submittedVersion)
- Funders
- Associazione Italiana per la Ricerca sul Cancro (15464, 15279, IG-15279)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Bioactive Compounds and Antitumor Agents
- Keywords
- Nrf2, Nrf2 signaling, oncogenic function, tumor suppressor, oxidative stress, chemoresistance, radioresistance (biology), Nrf2 inhibitors, therapeutic target, cancer
- MeSH terms
- Kelch-Like ECH-Associated Protein 1, Animals, Antineoplastic Agents, Humans, Mutation, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Oxidative Stress, MicroRNAs, Epigenesis, Genetic, NF-E2-Related Factor 2, Drug Discovery, Molecular Targeted Therapy
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