Evidence map›Paper›PMID 26497899›Full record

ArticleJournal of biomedical science2015

Epidermal growth factor receptor status and Notch inhibition in non-small cell lung cancer cells.

Efstathia Giannopoulou, Achilleas Nikolakopoulos, Dimitra Kotsirilou, Angeliki Lampropoulou, Sofia Raftopoulou, Evangelia Papadimitriou, Achilleas D Theocharis, Thomas Makatsoris, Konstantinos Fasseas, Haralabos P Kalofonos

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

10 authors at 2 institutions in 1 country.

Efstathia GiannopoulouClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece.
Achilleas NikolakopoulosClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece.
Dimitra KotsirilouClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece.
Angeliki LampropoulouClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece.
Sofia RaftopoulouElectron Microscopy Laboratory, Faculty of Crop Production, Agricultural University of Athens, Iera Odos 75, Athens, 11855, Greece.
Evangelia PapadimitriouLaboratory of Molecular Pharmacology, Department of Pharmacy, School of Health Science, University of Patras, Rio, 26504, Greece.
Achilleas D TheocharisLaboratory of Biochemistry, Department of Chemistry, University of Patras, Rio, 26504, Greece.
Thomas MakatsorisClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece.
Konstantinos FasseasElectron Microscopy Laboratory, Faculty of Crop Production, Agricultural University of Athens, Iera Odos 75, Athens, 11855, Greece.
Haralabos P KalofonosClinical Oncology Laboratory, Division of Oncology, Department of Medicine, University of Patras, Patras Medical School, Rio, 26504, Greece. kalofonos@upatras.gr.
University of Patras · GRAgricultural University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNotch may behave as an oncogene or a tumor suppressor gene in lung cancer cells. Notch receptor undergoes cleavage by enzymes, including γ-secretase, generating the active Notch intracellular domain (NICD). The aim of the present study was to investigate the effect of DAPT, a γ-secretase inhibitor, in non-small cell lung cancer (NSCLC) cells, as well as the impact of epidermal growth factor (EGF) that is over-expressed by NSCLC cells, on Notch signaling. H23, A549, H661 and HCC827 human NSCLC cell lines were used, expressing various NICD and EGF receptor (EGFR) protein levels.

resultsDAPT decreased the number of H661 cells in a concentration-dependent manner, while it had a small effect on H23 and A549 cells and no effect on HCC827 cells that carry mutated EGFR. Notch inhibition did not affect the stimulatory effect of EGF on cell proliferation, while EGF prevented DAPT-induced NICD decrease in H23 and H661 cells. The type of cell death induced by DAPT seems to depend on the cell type.

conclusionsOur data indicate that inhibition of Notch cleavage may not affect cell number in the presence of EGFR mutations and that EGFR may affect Notch signalling suggesting that a dual inhibition of these pathways might be promising in NSCLC.

Indexed as

MutationCarcinoma, Non-Small-Cell LungCell Line, TumorErbB ReceptorsHumansLung NeoplasmsReceptors, NotchSignal TransductionTumor Suppressor ProteinsEGFR protein, humanErbB ReceptorsReceptors, NotchTumor Suppressor Proteins

Identifiers

PMID26497899
PMCPMC4619334
OpenAlexW2153360462

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.