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NRF2 Promotes Tumor Maintenance by Modulating mRNA Translation in Pancreatic Cancer
Open accessAbstract
Pancreatic cancer is a deadly malignancy that lacks effective therapeutics. We previously reported that oncogenic Kras induced the redox master regulator Nfe2l2/Nrf2 to stimulate pancreatic and lung cancer initiation. Here, we show that NRF2 is necessary to maintain pancreatic cancer proliferation by regulating mRNA translation. Specifically, loss of NRF2 led to defects in autocrine epidermal growth factor receptor (EGFR) signaling and oxidation of specific translational regulatory proteins, resulting in impaired cap-dependent and cap-independent mRNA translation in pancreatic cancer cells. Combined targeting of the EGFR effector AKT and the glutathione antioxidant pathway mimicked Nrf2 ablation to potently inhibit pancreatic cancer ex vivo and in vivo, representing a promising synthetic lethal strategy for treating the disease.
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“For example, NRF2 steers glucose to anabolic cancer metabolism and prevents oxidation of multiple translational factors to augment protein output [15,16].”
From NRF2 Activation Confers Resistance to eIF4A Inhibitors in Cancer Therapy (2021) · cites this paper as [15]
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“Indeed, NRF2 is known to augment global protein production by reducing key translation factors such as eEF2 [15].”
From NRF2 Activation Confers Resistance to eIF4A Inhibitors in Cancer Therapy (2021) · cites this paper as [15]
In the citing paper
“For example, the transcription factor Nrf2, which mediates an antioxidant response program to detoxify ROS, is downstream of several oncogenic drivers, and loss of Nrf2 in this context can impair tumor proliferation (Chio et al., 2016; DeNicola et al., 2011).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Chio et al., 2016
In the citing paper
“In addition to activating the GOT2/GOT1/Malic Enzyme 1 (ME1) pathway, oncogenic KRAS activates the NRF2 antioxidant system by inducing NRF2 expression59,60 and by constitutively activating the battery of genes controlled by NRF2 to maintain the redox balance and promote tumorigenesis61.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [61]
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Metadata
- Authors
- Chio, I. I. C., Jafarnejad, S. M., Ponz-Sarvise, M., Park, Y., Rivera, K., Palm, W., Wilson, J., Sangar, V., Hao, Y., Öhlund, D., Wright, K., Filippini, D., Lee, E. J., Da Silva, B., Schoepfer, C., Wilkinson, J. E., Buscaglia, J. M., DeNicola, G. M., Tiriac, H., Hammell, M., Crawford, H. C., Schmidt, E. E., Thompson, C. B., Pappin, D. J., Sonenberg, N., & Tuveson, D. A.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- McGill University (CA)
- Memorial Sloan Kettering Cancer Center (US)
- Institute for Systems Biology (US)
- University of Michigan (US)
- Stony Brook School (US)
- Cornell University (US)
- Montana State University (US)
- Corresponding author
- Tuveson, David A.
- ORCID
- Chio, Iok In Christine
- Jafarnejad, Seyed Mehdi
- Park, Youngkyu
- Rivera, Keith
- Palm, Wilhelm
- Öhlund, Daniel
- Filippini, Dea
- Lee, Eun Jung
- Wilkinson, John Erby
- Buscaglia, Jonathan M.
- DeNicola, Gina M.
- Hammell, Molly
- Crawford, Howard C.
- Schmidt, Edward E.
- Thompson, Craig B.
- Pappin, Darryl J.
- Sonenberg, Nahum
- Tuveson, David A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 166
- Issue
- 4
- Pages
- 963-976
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5234705
- OpenAlex
- W2495582206
- Cited by
- 378
- References
- 60
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 31 · 2023: 54 · 2022: 35 · 2021: 54 · 2020: 42 · 2019: 40 · 2018: 43 · 2017: 40 · 2016: 9
- FWCI
- 22.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (submittedVersion)
- eScholarship@McGill (McGill) (submittedVersion, cc-by-nc-nd)
- Funders
- Cancer Center Support (5P30CA045508, P30CA008748)
- CSHL Association
- NIH (5P30CA45508-26, 5P50CA101955-07, 1U10CA180944-01, 5U01CA168409-3, 1R01CA190092-01, AG040020, CA152559, R01 CA159222)
- Carcinoid Foundation
- PCUK
- David Rubinstein Center for Pancreatic Cancer Research at MSKCC
- Stand Up to Cancer
- KWF
- STARR Foundation (I7-A718)
- DOD (W81XWH-13-PRCRP-IA)
- Precision Medicine Research Associates
- Damon Runyon Cancer Research Foundation (DRG-2165-13)
- Human Frontier Science Program (LT000190/2013)
- Cancer Research Society and CCSRI (702317)
- Canadian Institute of Health Research
- Swedish Research Council (537-2013-7277)
- Sociedad Española de Oncología Médica
- Hope Funds for Cancer Research Fellowship
- MSKCC Molecular Cytology Core
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- Nrf2, pancreatic cancer, mRNA translation, KRAS, EGFR signaling, autocrine signaling, protein oxidation, cap-dependent translation, cap-independent translation, Akt, synthetic lethality, tumor maintenance
- MeSH terms
- Animals, Cysteine, Glutathione, Humans, Organoids, Pancreatic Neoplasms, Protein Biosynthesis, Signal Transduction, Proto-Oncogene Proteins p21(ras), Autocrine Communication, NF-E2-Related Factor 2, Mice
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