Evidence map›Paper›PMID 24676055›Full record

ArticlePLoS genetics2014

FAK acts as a suppressor of RTK-MAP kinase signalling in Drosophila melanogaster epithelia and human cancer cells.

Juan Pablo Macagno, Jesica Diaz Vera, Yachuan Yu, Iain MacPherson, Emma Sandilands, Ruth Palmer, Jim C Norman, Margaret Frame, Marcos Vidal

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. TheeLife · 2026
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  9. [Influence of PTEN down-regulation by in vitro RNA interference on the migration of HSC-T6 cell line].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Article
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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 3 institutions in 2 countries.

Juan Pablo MacagnoCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Jesica Diaz VeraCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Yachuan YuCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Iain MacPhersonCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Emma SandilandsEdinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.
Ruth PalmerDepartment of Molecular Biology, Umeå University, Umeå, Sweden.
Jim C NormanCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Margaret FrameEdinburgh Cancer Research UK Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.
Marcos VidalCancer Research UK Beatson Institute, Garscube Estate, Glasgow, United Kingdom.
Cancer Research UK Scotland Institute · GBWestern General Hospital · GBUmeå University · SE

Funding

Cancer Research UK 15703Cancer Research UK 18277Cancer Research UK C596/A17196
6 · The paper itself

Abstract

Receptor Tyrosine Kinases (RTKs) and Focal Adhesion Kinase (FAK) regulate multiple signalling pathways, including mitogen-activated protein (MAP) kinase pathway. FAK interacts with several RTKs but little is known about how FAK regulates their downstream signalling. Here we investigated how FAK regulates signalling resulting from the overexpression of the RTKs RET and EGFR. FAK suppressed RTKs signalling in Drosophila melanogaster epithelia by impairing MAPK pathway. This regulation was also observed in MDA-MB-231 human breast cancer cells, suggesting it is a conserved phenomenon in humans. Mechanistically, FAK reduced receptor recycling into the plasma membrane, which resulted in lower MAPK activation. Conversely, increasing the membrane pool of the receptor increased MAPK pathway signalling. FAK is widely considered as a therapeutic target in cancer biology; however, it also has tumour suppressor properties in some contexts. Therefore, the FAK-mediated negative regulation of RTK/MAPK signalling described here may have potential implications in the designing of therapy strategies for RTK-driven tumours.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell ProliferationDrosophila melanogasterEpithelial CellsFemaleFocal Adhesion Kinase 1HumansMAP Kinase Signaling SystemPhosphorylationReceptor Protein-Tyrosine KinasesFocal Adhesion Kinase 1PTK2 protein, humanReceptor Protein-Tyrosine Kinases

Identifiers

PMID24676055
PMCPMC3967952
OpenAlexW2089359748

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.