ArticleThe American journal of pathology2010
The NADPH oxidase subunit p22phox inhibits the function of the tumor suppressor protein tuberin.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Targeting CYBA inhibits hepatic metastasis of pancreatic cancer through AKT/MLC2 pathway.Acta pharmacologica Sinica · 2026Article
- Resistance to the platinum‑based chemotherapeutic drugs in oral cancer: Focus on the role of p22phox (Review).Biomedical reports · 2024Review
- Integrated approach to reducing polypharmacy in older people: exploring the role of oxidative stress and antioxidant potential therapy.Redox report : communications in free radical research · 2024Review
- Inhibition of p22Journal of Cancer · 2021Article
- Nuclear NADPH oxidase-4 associated with disease progression in renal cell carcinoma.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Glutathione S-Transferase Mu-3 Predicts a Better Prognosis and Inhibits Malignant Behavior and Glycolysis in Pancreatic Cancer.Frontiers in oncology · 2020Article
- Article
- A novel functional polymorphism of GSTM3 reduces clear cell renal cell carcinoma risk through enhancing its expression by interfering miR-556 binding.Journal of cellular and molecular medicine · 2018Article
- Nox4 is a Target for Tuberin Deficiency Syndrome.Scientific reports · 2018Article
- NOX4 functions as a mitochondrial energetic sensor coupling cancer metabolic reprogramming to drug resistance.Nature communications · 2017Article
- Renal Carcinogenesis, Tumor Heterogeneity, and Reactive Oxygen Species: Tactics Evolved.Antioxidants & redox signaling · 2016Review
- Article
- NOX1 supports the metabolic remodeling of HepG2 cells.PloS one · 2015Article
- NADPH oxidase NOX4 supports renal tumorigenesis by promoting the expression and nuclear accumulation of HIF2α.Cancer research · 2014Article
- Mammalian target of rapamycin regulates Nox4-mediated podocyte depletion in diabetic renal injury.Diabetes · 2013Article
- Stabilization of HIF-2α through redox regulation of mTORC2 activation and initiation of mRNA translation.Oncogene · 2013Article
- NADPH-oxidase 4 protects against kidney fibrosis during chronic renal injury.Journal of the American Society of Nephrology : JASN · 2012Article
- Aiding and abetting roles of NOX oxidases in cellular transformation.Nature reviews. Cancer · 2012Review
- The NOX toolbox: validating the role of NADPH oxidases in physiology and disease.Cellular and molecular life sciences : CMLS · 2012Review
- The roles of beta-adrenergic receptors in tumorigenesis and the possible use of beta-adrenergic blockers for cancer treatment: possible genetic and cell-signaling mechanisms.Cancer management and research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the von Hippel-Lindau (VHL) gene give rise to renal cell carcinoma. Reactive oxygen species, generated by Nox oxidases, are involved in tumorigenesis. We have previously demonstrated that in VHL-deficient cells, p22(phox)-dependent Nox1 and Nox4 oxidases maintain hypoxia inducible factor-2alpha (HIF-2alpha) protein expression through an Akt-dependent translational pathway. Phosphorylation of tuberin, by Akt, results in its inactivation. Here we show that diphenyleneiodonium chloride, an inhibitor of Nox oxidases, and small-interfering RNA-mediated down-regulation of p22(phox) inhibit Akt-dependent phosphorylation of tuberin and stabilizes tuberin protein levels in VHL-deficient renal carcinoma cells. p22(phox)-mediated inactivation of tuberin is associated with an increase in ribosomal protein S6 kinase 1 and eukaryotic initiation factor 4E-binding protein-1 (4E-BP1) phosphorylation as well as HIF-2alpha stabilization. Importantly, we find that marked up-regulation of p22(phox) in human renal cell carcinoma correlates with increased tuberin phosphorylation, decreased tuberin protein levels, and increased phosphorylation of 4E-BP1. Our data provide the first evidence that p22(phox)-based Nox oxidases maintain HIF-2alpha protein expression through inactivation of tuberin and downstream activation of ribosomal protein S6 kinase 1/4E-BP1 pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.