Evidence map›Paper›PMID 27096894›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Modulation of membrane properties of lung cancer cells by azurin enhances the sensitivity to EGFR-targeted therapy and decreased β1 integrin-mediated adhesion.

Nuno Bernardes, Sofia Abreu, Filomena A Carvalho, Fábio Fernandes, Nuno C Santos, Arsénio M Fialho

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. The Production of Recombinant Azurin fromInternational journal of molecular sciences · 2025
    Article
  4. Review
  5. Review
  6. Interaction ofInternational journal of molecular sciences · 2025
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  7. Article
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  13. Article
  14. The concurrent effects of3 Biotech · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Nuno Bernardesa iBB-Institute for Bioengineering and Biosciences, Biological Sciences Research Group , Lisbon , Portugal.
Sofia Abreua iBB-Institute for Bioengineering and Biosciences, Biological Sciences Research Group , Lisbon , Portugal.
Filomena A Carvalhob Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa , Lisbon , Portugal.
Fábio Fernandesc Centro de Quimica-Fisica Molecular, Instituto Superior Técnico , Lisbon , Portugal.
Nuno C Santosb Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa , Lisbon , Portugal.
Arsénio M Fialhoa iBB-Institute for Bioengineering and Biosciences, Biological Sciences Research Group , Lisbon , Portugal.
Institute for Biotechnology and Bioengineering · PTUniversity of Lisbon · PTInstituto Superior Técnico

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In lung cancer, the Epidermal Growth Factor Receptor (EGFR) is one of the main targets for clinical management of this disease. The effectiveness of therapies toward this receptor has already been linked to the expression of integrin receptor subunit β1 in NSCLC A549 cells. In this work we demonstrate that azurin, an anticancer therapeutic protein originated from bacterial cells, controls the levels of integrin β1 and its appropriate membrane localization, impairing the intracellular signaling cascades downstream these receptors and the invasiveness of cells. We show evidences that azurin when combined with gefitinib and erlotinib, tyrosine kinase inhibitors which targets specifically the EGFR, enhances the sensitivity of these lung cancer cells to these molecules. The broad effect of azurin at the cell surface level was examined by Atomic Force Microscopy. The Young 's module (E) shows that the stiffness of A549 lung cancer cells decreased with exposure to azurin and also gefitinib, suggesting that the alterations in the membrane properties may be the basis of the broad anticancer activity of this protein. Overall, these results show that azurin may be relevant as an adjuvant to improve the effects of other anticancer agents already in clinical use, to which patients often develop resistance hampering its full therapeutic response.

Indexed as

A549 CellsAntineoplastic AgentsAzurinBacterial ProteinsCell AdhesionCell MembraneCell MovementCell ProliferationDrug SynergismElastic ModulusErbB ReceptorsErlotinib HydrochlorideExtracellular MatrixGefitinibGene ExpressionHumansAntineoplastic AgentsAzurinBacterial ProteinsEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideGefitinibIntegrin beta1Quinazolinesatomic force microscoyazurinEGFRgefitinibintegrinNSCLCβ1

Identifiers

PMID27096894
PMCPMC4934055
OpenAlexW2338846502

What OpenQuestion holds

Textmetadata
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.