ArticleCancer research2014
NADPH oxidase NOX4 supports renal tumorigenesis by promoting the expression and nuclear accumulation of HIF2α.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- CBX4 and NOX4 Expression Are Associated With Chemoradiotherapy Response and Overall Survival in Locally Advanced Cervical Squamous Cell Carcinoma.Cancer medicine · 2026Article
- Genetic and Pharmacological Inhibition of NOX4 Protects Against Rhabdomyolysis-Induced Acute Kidney Injury Through Suppression of Endoplasmic Reticulum Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and therapeutic prospects.Cancer cell international · 2025Review
- NADPH Oxidase 4 (NOX4) in Cancer: Linking Redox Signals to Oncogenic Metabolic Adaptation.International journal of molecular sciences · 2022Review
- MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway.Cancer cell international · 2022Article
- MicroRNA-100 Enhances Autophagy and Suppresses Migration and Invasion of Renal Cell Carcinoma Cells via Disruption of NOX4-Dependent mTOR Pathway.Clinical and translational science · 2022Article
- Potential Key Markers for Predicting the Prognosis of Gastric Adenocarcinoma Based on the Expression of Ferroptosis-Related lncRNA.Journal of immunology research · 2022Article
- NADPH Oxidase 4: A Potential Therapeutic Target of Malignancy.Frontiers in cell and developmental biology · 2022Review
- NOX4: a potential therapeutic target for pancreatic cancer and its mechanism.Journal of translational medicine · 2021Review
- Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021Review
- Article
- Intratumoral Fibrosis in Facilitating Renal Cancer Aggressiveness: Underlying Mechanisms and Promising Targets.Frontiers in cell and developmental biology · 2021Review
- Gallbladder cancer-associated fibroblasts promote vasculogenic mimicry formation and tumor growth in gallbladder cancer via upregulating the expression of NOX4, a poor prognosis factor, through IL-6-JAK-STAT3 signal pathway.Journal of experimental & clinical cancer research : CR · 2020Article
- Beyond glycolysis: Hypoxia signaling as a master regulator of alternative metabolic pathways and the implications in clear cell renal cell carcinoma.Cancer letters · 2020Review
- Nuclear NADPH oxidase-4 associated with disease progression in renal cell carcinoma.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Increased formation of reactive oxygen species during tumor growth: Ex vivo low-temperature EPR and in vivo bioluminescence analyses.Free radical biology & medicine · 2020Article
- Mechanisms of hypoxia signalling: new implications for nephrology.Nature reviews. Nephrology · 2019Review
- Article
- Accumulation of fructose 1,6-bisphosphate protects clear cell renal cell carcinoma from oxidative stress.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Integrative analysis of cancer driver genes in prostate adenocarcinoma.Molecular medicine reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Most sporadically occurring renal tumors include a functional loss of the tumor suppressor von Hippel Lindau (VHL). Development of VHL-deficient renal cell carcinoma (RCC) relies upon activation of the hypoxia-inducible factor-2α (HIF2α), a master transcriptional regulator of genes that drive diverse processes, including angiogenesis, proliferation, and anaerobic metabolism. In determining the critical functions for HIF2α expression in RCC cells, the NADPH oxidase NOX4 has been identified, but the pathogenic contributions of NOX4 to RCC have not been evaluated directly. Here, we report that NOX4 silencing in VHL-deficient RCC cells abrogates cell branching, invasion, colony formation, and growth in a murine xenograft model RCC. These alterations were phenocopied by treatment of the superoxide scavenger, TEMPOL, or by overexpression of manganese superoxide dismutase or catalase. Notably, NOX4 silencing or superoxide scavenging was sufficient to block nuclear accumulation of HIF2α in RCC cells. Our results offer direct evidence that NOX4 is critical for renal tumorigenesis and they show how NOX4 suppression and VHL re-expression in VHL-deficient RCC cells are genetically synonymous, supporting development of therapeutic regimens aimed at NOX4 blockade.
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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.