Evidence map›Paper›PMID 25806803›Full record

ArticlePloS one2015

NOX1 supports the metabolic remodeling of HepG2 cells.

Katharina Bertram, Cristina-Maria Valcu, Michael Weitnauer, Uwe Linne, Agnes Görlach

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Inhibiting the Activity of NADPH Oxidase in Cancer.Antioxidants & redox signaling · 2020
    Article
  10. Article
  11. Review
  12. Review
  13. Therapeutic potential of NADPH oxidase 1/4 inhibitors.British journal of pharmacology · 2017
    Review
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Katharina BertramExperimental and Molecular Paediatric Cardiology, German Heart Centre Munich at the Technical University Munich, Lazarettstr. 36, Munich, Germany.
Cristina-Maria ValcuExperimental and Molecular Paediatric Cardiology, German Heart Centre Munich at the Technical University Munich, Lazarettstr. 36, Munich, Germany.
Michael WeitnauerExperimental and Molecular Paediatric Cardiology, German Heart Centre Munich at the Technical University Munich, Lazarettstr. 36, Munich, Germany.
Uwe LinneChemistry Department-Mass Spectrometry, Philipps-University Marburg, Hans-Meerwein-Strasse, Marburg, Germany.
Agnes GörlachExperimental and Molecular Paediatric Cardiology, German Heart Centre Munich at the Technical University Munich, Lazarettstr. 36, Munich, Germany.
Deutsches Herzzentrum München · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NADPH oxidases are important sources of reactive oxygen species (ROS) which act as signaling molecules in the regulation of protein expression, cell proliferation, differentiation, migration and cell death. The NOX1 subunit is over-expressed in several cancers and NOX1 derived ROS have been repeatedly linked with tumorigenesis and tumor progression although underlying pathways are ill defined. We engineered NOX1-depleted HepG2 hepatoblastoma cells and employed differential display 2DE experiments in order to investigate changes in NOX1-dependent protein expression profiles. A total of 17 protein functions were identified to be dysregulated in NOX1-depleted cells. The proteomic results support a connection between NOX1 and the Warburg effect and a role for NOX in the regulation of glucose and glutamine metabolism as well as of lipid, protein and nucleotide synthesis in hepatic tumor cells. Metabolic remodeling is a common feature of tumor cells and understanding the underlying mechanisms is essential for the development of new cancer treatments. Our results reveal a manifold involvement of NOX1 in the metabolic remodeling of hepatoblastoma cells towards a sustained production of building blocks required to maintain a high proliferative rate, thus rendering NOX1 a potential target for cancer therapy.

Indexed as

Down-RegulationElectrophoresis, Gel, Two-DimensionalGlucoseGlutamineHep G2 CellsHumansLipid MetabolismMetabolic Networks and PathwaysNADPH Oxidase 1NADPH OxidasesProteinsReactive Oxygen SpeciesRNA InterferenceRNA, Small InterferingTandem Mass SpectrometryUp-RegulationGlucoseGlutamineNADPH Oxidase 1NADPH OxidasesNOX1 protein, humanProteinsReactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID25806803
PMCPMC4373763
OpenAlexW2114213013

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.