Evidence map›Paper›PMID 27153109›Full record

ArticlePloS one2016

EGFR Activation Leads to Cell Death Independent of PI3K/AKT/mTOR in an AD293 Cell Line.

Cezary Treda, Marta Popeda, Magdalena Ksiazkiewicz, Dawid P Grzela, Maciej P Walczak, Mateusz Banaszczyk, Joanna Peciak, Ewelina Stoczynska-Fidelus, Piotr Rieske

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. A review of theFrontiers in pharmacology · 2024
    Review
  5. Article
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  16. Article
  17. Review
  18. Article
  19. Article
  20. EGFRJournal of oncology · 2019
    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

9 authors at 1 institution in 1 country.

Cezary TredaDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.ORCID 0000-0002-7911-788X
Marta PopedaDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Magdalena KsiazkiewiczDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Dawid P GrzelaDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Maciej P WalczakDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Mateusz BanaszczykDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Joanna PeciakDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Ewelina Stoczynska-FidelusDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Piotr RieskeDepartment of Research and Development, Celther Polska Ltd., Lodz, Poland.
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Epidermal Growth Factor Receptor (EGFR) and its mutations contribute in various ways to tumorigenesis and biology of human cancers. They are associated with tumor proliferation, progression, drug resistance and the process of apoptosis. There are also reports that overexpression and activation of wild-type EGFR may lead to cell apoptosis. To study this phenomenon, we overexpressed in an AD293 cell line two most frequently observed forms of the EGFR receptor: wild-type and the constitutively active mutant-EGFR variant III (EGFRvIII). Then, we compared the effect of EGF stimulation on cell viability and downstream EGFR signaling. AD293 cells overexpressing wild-type EGFR, despite a significant proliferation increase in serum supplemented medium, underwent apoptosis after EGF stimulation in serum free conditions. EGFRvIII expressing cells, however, were unaffected by either serum starvation or EGF treatment. The effect of EGF was completely neutralized by tyrosine kinase inhibitors (TKIs), indicating the specificity of this observation. Moreover, apoptosis was not prevented by inhibiting EGFR downstream proteins (PI3K, AKT and mTOR). Here we showed another EGFR function, dependent on environmental factors, which could be employed in therapy and drug design. We also proposed a new tool for EGFR inhibitor analysis.

Indexed as

ApoptosisCell AdhesionCell LineCell ProliferationEpidermal Growth FactorErbB ReceptorsHumansPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesEpidermal Growth FactorErbB ReceptorsMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID27153109
PMCPMC4859505
OpenAlexW2346179791

What OpenQuestion holds

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LicenceCC BY
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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.