ReviewBiophysical reviews2020
Metabolic features of cancer cells in NRF2 addiction status.
Review in Biophysical reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Molecular mechanisms and targeted therapeutic strategies for glycolytic reprogramming in osteosarcoma.Genes & diseases · 2027Review
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- NRF2 activation in cancer and overview of NRF2 small molecule inhibitors.Archives of pharmacal research · 2025Review
- Therapeutic potential of NRF2 activating drug RTA-408 in suppressing T cell effector responses and inflammatory bowel disease.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A Review Unveiling the Ferroptosis-Regulated Cell Signalling Pathways in Breast Cancer to Elucidate Potent Targets for Cancer Management.Current pharmaceutical design · 2025Review
- Review
- PPIA dictates NRF2 stability to promote lung cancer progression.Nature communications · 2024Article
- A dual model of normal vs isogenic Nrf2-depleted murine epithelial cells to explore oxidative stress involvement.Scientific reports · 2024Article
- The Growth Inhibitory Effect of Resveratrol and Gallic Acid on Prostate Cancer Cell Lines through the Alteration of Oxidative Stress Balance: The Interplay betweenAnti-cancer agents in medicinal chemistry · 2024Article
- How to deal with frenemy NRF2: Targeting NRF2 for chemoprevention and cancer therapy.Journal of food and drug analysis · 2023Review
- Contribution of NRF2 to sulfur metabolism and mitochondrial activity.Redox biology · 2023Article
- Emerging Role of NRF2 Signaling in Cancer Stem Cell Phenotype.Molecules and cells · 2023Review
- Review
- Deregulated transcription factors in cancer cell metabolisms and reprogramming.Seminars in cancer biology · 2022Review
- Heterogeneity of the cancer cell line metabolic landscape.Molecular systems biology · 2022Article
- Oxidative Stress and Cancer Heterogeneity Orchestrate NRF2 Roles Relevant for Therapy Response.Molecules (Basel, Switzerland) · 2022Review
- Carbon Monoxide-Releasing Molecule-3 Suppresses the Malignant Biological Behavior of Tongue Squamous Cell Carcinoma via Regulating Keap1/Nrf2/HO-1 Signaling Pathway.BioMed research international · 2022Article
- Dietary Phytochemicals Targeting Nrf2 to Enhance the Radiosensitivity of Cancer.Oxidative medicine and cellular longevity · 2022Review
- Role of Nrf2 Signaling Cascade in Breast Cancer: Strategies and Treatment.Frontiers in pharmacology · 2022Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The KEAP1-NRF2 system is a sulfur-employing defense mechanism against oxidative and electrophilic stress. NRF2 is a potent transcription activator for genes mediating sulfur-involving redox reactions, and KEAP1 controls the NRF2 activity in response to the stimuli by utilizing reactivity of sulfur atoms. In many human cancer cells, the KEAP1-mediated regulation of NRF2 activity is abrogated, resulting in the persistent activation of NRF2. Persistently activated NRF2 drives malignant progression of cancers by increasing therapeutic resistance and promoting aggressive tumorigenesis, a state termed as NRF2 addiction. In NRF2-addicted cancer cell, NRF2 contributes to metabolic reprogramming in cooperation with other oncogenic pathways. In particular, NRF2 strongly activates cystine uptake coupled with glutamate excretion and glutathione synthesis, which increases consumption of intracellular glutamate. Decreased availability of glutamate limits anaplerosis of the TCA cycle, resulting in low mitochondrial respiration, and nitrogen source, resulting in the high dependency on exogenous non-essential amino acids. The highly enhanced glutathione synthesis is also likely to alter sulfur metabolism, which can contribute to the maintenance of the mitochondrial membrane potential in normal cells. The potent antioxidant and detoxification capacity supported by abundant production of glutathione is achieved at the expense of central carbon metabolism and requires skewed metabolic flow of sulfur. These metabolic features of NRF2 addiction status provide clues for novel therapeutic strategies to target NRF2-addicted cancer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.