Evidence map›Paper›PMID 25118939›Full record

ArticleCell death & disease2014

FAK competes for Src to promote migration against invasion in melanoma cells.

K Kolli-Bouhafs, E Sick, F Noulet, J-P Gies, J De Mey, P Rondé

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

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  7. Adaptor Protein ShcD/Molecular cancer research : MCR · 2021
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  11. NHCancer science · 2020
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  19. (Arg)Journal of experimental & clinical cancer research : CR · 2018
    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

6 authors at 3 institutions in 1 country.

K Kolli-Bouhafs1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
E Sick1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
F Noulet1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
J-P Gies1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
J De Mey1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
P Rondé1] CNRS, UMR 7213, Laboratoire de Biophotonique et Pharmacologie, Illkirch, France [2] Université de Strasbourg, Faculté de Pharmacie, Illkirch, France.
Centre National de la Recherche Scientifique · FRLaboratoire de Biophotonique et Pharmacologie · FRUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is one of the most deadly cancers because of its high propensity to metastasis, a process that requires migration and invasion of tumor cells driven by the regulated formation of adhesives structures like focal adhesions (FAs) and invasive structures like invadopodia. FAK, the major kinase of FAs, has been implicated in many cellular processes, including migration and invasion. In this study, we investigated the role of FAK in the regulation of invasion. We report that suppression of FAK in B16F10 melanoma cells led to increased invadopodia formation and invasion through Matrigel, but impaired migration. These effects are rescued by FAK WT but not by FAK(Y397F) reexpression. Invadopodia formation requires local Src activation downstream of FAK and in a FAK phosphorylation-dependant manner. FAK deletion correlates with increased phosphorylation of Tks-5 (tyrosine kinase substrate with five SH3 domain) and reactive oxygen species production. In conclusion, our data show that FAK is able to mediate opposite effects on cell migration and invasion. Accordingly, beneficial effects of FAK inhibition are context dependent and may depend on the cell response to environmental cues and/or on the primary or secondary changes that melanoma experienced through the invasion cycle.

Indexed as

AnimalsCell Line, TumorCell MovementFocal Adhesion Kinase 1MelanomaMetalloporphyrinsMicePhosphate-Binding ProteinsPhosphoproteinsPhosphorylationPyrimidinesReactive Oxygen SpeciesRNA InterferenceRNA, Small Interferingsrc-Family KinasesAG 1879Fish protein, mouseFocal Adhesion Kinase 1MetalloporphyrinsMn(III) 5,10,15,20-tetrakis(N-methylpyridinium-2-yl)porphyrinPhosphate-Binding ProteinsPhosphoproteinsPtk2 protein, mousePyrimidinesReactive Oxygen SpeciesRNA, Small Interferingsrc-Family Kinases

Identifiers

PMID25118939
PMCPMC4454304
OpenAlexW2052470057

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.