Evidence map›Paper›PMID 26238631›Full record

ArticleMolecular oncology2015

PEA3 transcription factors are downstream effectors of Met signaling involved in migration and invasiveness of Met-addicted tumor cells.

Zoulika Kherrouche, Didier Monte, Elisabeth Werkmeister, Luc Stoven, Yvan De Launoit, Alexis B Cortot, David Tulasne, Anne Chotteau-Lelievre

Open access · bronzeAbstract read
In one paragraph

Article in Molecular oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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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

8 authors at 1 institution in 2 countries.

Zoulika KherroucheCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France.
Didier MonteCNRS USR 3078, Institut de Recherche Interdisciplinaire, Université de Lille, Villeneuve d'Ascq 59658, France.
Elisabeth WerkmeisterCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France; BioImaging Center Lille Nord de France, Lille 59021, France.
Luc StovenCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France.
Yvan De LaunoitCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France.
Alexis B CortotCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France; Thoracic Oncology Department, Lille University Hospital, Université de Lille, France.
David TulasneCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France. Electronic address: david.tulasne@ibl.cnrs.fr.
Anne Chotteau-LelievreCNRS UMR 8161, Institut de Biologie de Lille, Institut Pasteur de Lille, Université de Lille, SIRIC ONCOLille, Lille 59021, France.
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various solid tumors including lung or gastric carcinomas display aberrant activation of the Met receptor which correlates with aggressive phenotypes and poor prognosis. Although downstream signaling of Met is well described, its integration at the transcriptional level is poorly understood. We demonstrate here that in cancer cells harboring met gene amplification, inhibition of Met activity with tyrosine kinase inhibitors or specific siRNA drastically decreased expression of ETV1, ETV4 and ETV5, three transcription factors constituting the PEA3 subgroup of the ETS family, while expression of the other members of the family were less or not affected. Similar link between Met activity and PEA3 factors expression was found in lung cancer cells displaying resistance to EGFR targeted therapy involving met gene amplification. Using silencing experiments, we demonstrate that the PEA3 factors are required for efficient migration and invasion mediated by Met, while other biological responses such as proliferation or unanchored growth remain unaffected. PEA3 overexpression or silencing revealed that they participated in the regulation of the MMP2 target gene involved in extracellular matrix remodeling. Our results demonstrated that PEA3-subgroup transcription factors are key players of the Met signaling integration involved in regulation of migration and invasiveness.

Indexed as

Signal TransductionCell Line, TumorCell MovementGene AmplificationGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessNeoplasmsProto-Oncogene Proteins c-metTranscription FactorsMET protein, humanProto-Oncogene Proteins c-mettranscription factor PEA3Transcription FactorsEGFRETSLung tumorigenesisMetMigrationPEA3Receptor tyrosine kinaseTranscription factor

Identifiers

PMID26238631
PMCPMC5528715
OpenAlexW1899730350

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.