Evidence map›Paper›PMID 24911159›Full record

ArticlePloS one2014

Redox modulation of FAK controls melanoma survival--role of NOX4.

Cristiane Ribeiro-Pereira, João Alfredo Moraes, Mariele de Jesus Souza, Francisco R Laurindo, Maria Augusta Arruda, Christina Barja-Fidalgo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Redox-Related Proteins in Melanoma Progression.Antioxidants (Basel, Switzerland) · 2022
    Article
  10. Frontiers in cellular and infection microbiology · 2022
    Article
  11. Review
  12. The Interplay between HGF/c-met Axis and Nox4 in BRAF Mutated Melanoma.International journal of molecular sciences · 2021
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 1 country.

Cristiane Ribeiro-PereiraLaboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
João Alfredo MoraesLaboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Mariele de Jesus SouzaLaboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Francisco R LaurindoLaboratory of Vascular Biology, Instituto do Coração, Universidade de São Paulo, São Paulo, SP, Brazil.
Maria Augusta ArrudaLaboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil; Vice-Diretoria de Ensino, Pesquisa e Inovação, Farmanguinhos, Fiocruz, Rio de Janeiro, RJ, Brazil.
Christina Barja-FidalgoLaboratory of Cellular and Molecular Pharmacology, Department of Cell Biology, IBRAG, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Universidade do Estado do Rio de Janeiro · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies have demonstrated that reactive oxygen species (ROS) generated by NADPH oxidase are essential for melanoma proliferation and survival. However, the mechanisms by which NADPH oxidase regulates these effects are still unclear. In this work, we investigate the role of NADPH oxidase-derived ROS in the signaling events that coordinate melanoma cell survival. Using the highly metastatic human melanoma cell line MV3, we observed that pharmacological NADPH oxidase inhibition reduced melanoma viability and induced dramatic cellular shape changes. These effects were accompanied by actin cytoskeleton rearrangement, diminished FAKY397 phosphorylation, and decrease of FAK-actin and FAK-cSrc association, indicating disassembly of focal adhesion processes, a phenomenon that often results in anoikis. Accordingly, NADPH oxidase inhibition also enhanced hypodiploid DNA content, and caspase-3 activation, suggesting activation of the apoptotic machinery. NOX4 is likely to be involved in these effects, since silencing of NOX4 significantly inhibited basal ROS production, reduced FAKY397 phosphorylation and decreased tumor cell viability. Altogether, the results suggest that intracellular ROS generated by the NADPH oxidase, most likely NOX4, transmits cell survival signals on melanoma cells through the FAK pathway, maintaining adhesion contacts and cell viability.

Indexed as

Oxidation-ReductionActinsApoptosisCell AdhesionCell Line, TumorCell SurvivalCSK Tyrosine-Protein KinaseEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesGene SilencingHumansIntracellular SpaceMelanomaNADPH Oxidase 4NADPH OxidasesPhosphorylationActinsCSK protein, humanCSK Tyrosine-Protein KinaseFocal Adhesion Protein-Tyrosine KinasesNADPH Oxidase 4NADPH OxidasesNOX4 protein, humanReactive Oxygen Speciessrc-Family Kinases

Identifiers

PMID24911159
PMCPMC4050056
OpenAlexW2043666859

What OpenQuestion holds

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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.