CUL3 and NRF2 Mutations Confer an NRF2 Activation Phenotype in a Sporadic Form of Papillary Renal Cell Carcinoma

Ooi, Aikseng; Dykema, Karl; Ansari, Asif; Petillo, David; Snider, John; Kahnoski, Richard; Anema, John; Craig, David; Carpten, John; Teh, Bin-Tean; Furge, Kyle A.

doi:10.1158/0008-5472.can-12-3227

Cited by 159Genomics, phytochemicals, and oxidative stressRenal cell carcinoma treatmentChromatin Remodeling and Cancer

CUL3 and NRF2 Mutations Confer an NRF2 Activation Phenotype in a Sporadic Form of Papillary Renal Cell Carcinoma

Ooi, Aikseng, Dykema, Karl, Ansari, Asif, Petillo, David, Snider, John, Kahnoski, Richard, Anema, John, Craig, David +3 more·2013·Cancer Research

DOI 10.1158/0008-5472.can-12-3227

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Abstract

Sustained activation of the stress-regulated transcription factor NRF2 (NFE2L2) is a prominent feature of many types of cancer, implying that mutations driving NRF2 may be important to tumor progression. In hereditary type 2 papillary renal cell carcinoma (PRCC2, also known as hereditary leiomyomatosis and renal cell cancer), NRF2 activation is a direct consequence of the accumulation of intracellular fumarate, a result of fumarate hydratase (FH) inactivation, but it is not clear how NRF2 may be activated in sporadic forms of PRCC2. Here we show that somatic mutations in NRF2, CUL3, and SIRT1 are responsible for driving the NRF2 activation phenotype in sporadic PRCC2. Transcriptome sequencing revealed the expression pattern of mutant alleles of NRF2, CUL3, and SIRT1 and also confirmed NRF2 activation in clinical specimens. Our results show a convergence in somatic mutations in sporadic PRCC2 with FH mutation in hereditary PRCC2. Cancer Res; 73(7); 2044–51. ©2013 AACR.

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Some somatic mutations give rise to hyperactive Nrf2, which causes enhanced antioxidant capacity and confers protection of cancer cells from ROS and cancer therapy, leading to cancer cell growth and proliferation, cancer progression, and cancer therapy resistance.
“Some somatic mutations give rise to hyperactive Nrf2, which causes enhanced antioxidant capacity and confers protection of cancer cells from ROS and cancer therapy, thereby leading to cancer cell growth and proliferation, cancer progression, and cancer therapy resistance (e.g., chemoresistance) (Figure 8) [161,162,163,164,165,166,167,168,169,170,171].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [166]
Most of these cancers' aberrant Nrf2 expression and poor prognosis have been attributed to loss-of-function mutations in KEAP1 and/or gain-of-function mutations in NFE2L2.
“most of which have been attributed to loss-of-function mutations in the KEAP1 gene and/or gain-of-function mutations in the NFE2L2 gene encoding Nrf2 [162,163,164,166,167].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [166]

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Abstract 1134: Fumarate activates NRF2 in tissues with fumarate hydratase mutation
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Self-citation
Abstract 3820: Deregulation of KEAP1-NRF axis in phenotypically type 2 papillary renal cell carcinoma
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Molecular characterization of hereditary and sporadic papillary renal cell carcinoma type 2 (PRCC2)
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Sustained NRF2 activation in hereditary leiomyomatosis and renal cell cancer (HLRCC) and in hereditary tyrosinemia type 1 (HT1)
Sandhu, I. S., Maksim, N. J., Amouzougan, E. A., Gallion, B. W., Raviele, A. L. J., & Ooi, A. (2015) · Biochemical Society Transactions · doi:10.1042/bst20150041 · Cited by 19 · see citing works
Self-citation

Authors: Ooi, A., Dykema, K., Ansari, A., Petillo, D., Snider, J., Kahnoski, R., Anema, J., Craig, D., Carpten, J., Teh, B.-T., & Furge, K. A.
Affiliations: Van Andel Institute (US)
ORCID: Petillo, David
Kahnoski, Richard
Craig, David
Carpten, John
Teh, Bin-Tean
Venue: Cancer Research
Publisher: American Association for Cancer Research (AACR)
Published: 2013-04-01
Volume: 73
Issue: 7
Pages: 2044-2051
ISSN: 0008-5472 (ISSN-L)
1538-7445
DOI: 10.1158/0008-5472.can-12-3227
OpenAlex: W2135514225
Cited by: 159
References: 35
Citations by year: 2026: 3 · 2025: 7 · 2024: 6 · 2023: 7 · 2022: 13 · 2021: 9 · 2020: 19 · 2019: 17 · 2018: 13 · 2017: 11 · 2016: 12 · 2015: 20 · 2014: 13 · 2013: 8 · 2012: 1
FWCI: 7.91
Type: journal article
Language: en
Open access: closed
Locations: Cancer Research (publishedVersion)
PubMed (publishedVersion)
National University of Singapore (submittedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal cell carcinoma treatment
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: papillary renal cell carcinoma, Nrf2 activation, CUL3, NRF2 mutation, SIRT1, fumarate hydratase, hereditary leiomyomatosis and renal cell carcinoma, somatic mutations, fumarate accumulation, tumor progression
MeSH terms: Kelch-Like ECH-Associated Protein 1, Amino Acid Sequence, Carcinoma, Renal Cell, Cells, Cultured, Humans, Immunoenzyme Techniques, Kidney Neoplasms, Kidney Tubules, Proximal, Molecular Sequence Data, Mutation, Phenotype, Biomarkers, Tumor, Blotting, Western, Sequence Homology, Amino Acid, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Cullin Proteins, Intracellular Signaling Peptides and Proteins, NF-E2-Related Factor 2, Sirtuin 1, High-Throughput Nucleotide Sequencing

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CUL3 and NRF2 Mutations Confer an NRF2 Activation Phenotype in a Sporadic Form of Papillary Renal Cell Carcinoma

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