Evidence map›Paper›PMID 32633461›Full record

ArticleJournal of cellular and molecular medicine2020

LIX1 regulates YAP activity and controls gastrointestinal cancer cell plasticity.

Amandine Guérin, Delphine Martire, Eva Trenquier, Tom Lesluyes, Sébastien Sagnol, Marine Pratlong, Elise Lefebvre, Fréderic Chibon, Pascal de Santa Barbara, Sandrine Faure

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. 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
1.0field-weighted citation impact, top 28% 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, 13 citations in OpenAlex.

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  8. Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022
    Review
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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

10 authors at 1 institution in 1 country.

Amandine GuérinPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.
Delphine MartirePhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.
Eva TrenquierPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.
Tom LesluyesCancer Research Center of Toulouse, University of Toulouse, INSERM, CNRS, Toulouse, France.
Sébastien SagnolPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.
Marine PratlongMGX, Biocampus Montpellier, CNRS, INSERM, University of Montpellier, Montpellier, France.
Elise LefebvreMGX, Biocampus Montpellier, CNRS, INSERM, University of Montpellier, Montpellier, France.
Fréderic ChibonCancer Research Center of Toulouse, University of Toulouse, INSERM, CNRS, Toulouse, France.
Pascal de Santa BarbaraPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.ORCID 0000-0001-9040-2481
Sandrine FaurePhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.ORCID 0000-0002-8902-8274
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal stromal tumours (GISTs), the most common mesenchymal neoplasm of the gastrointestinal tract, result from deregulated proliferation of transformed KIT-positive interstitial cells of Cajal that share mesenchymal progenitors with smooth muscle cells. Despite the identification of selective KIT inhibitors, primary resistance and relapse remain a major concern. Moreover, most patients develop resistance partly through reactivation of KIT and its downstream signalling pathways. We previously identified the Limb Expression 1 (LIX1) gene as a unique marker of digestive mesenchyme immaturity. We also demonstrated that LIX1 regulates mesenchymal progenitor proliferation and differentiation by controlling the Hippo effector YAP1, which is constitutively activated in many sarcomas. Therefore, we wanted to determine LIX1 role in GIST development. We found that LIX1 is strongly up-regulated in GIST samples and this is associated with unfavourable prognosis. Moreover, LIX1 controls GIST cell proliferation in vitro and in vivo. Upon LIX1 inactivation in GIST cells, YAP1/TAZ activity is reduced, KIT (the GIST signature) is down-regulated, and cells acquire smooth muscle lineage features. Our data highlight LIX1 role in digestive mesenchyme-derived cell-fate decisions and identify this novel regulator as a target for drug design for GIST treatment by influencing its differentiation status.

Indexed as

Cell PlasticityAnimalsAutophagy-Related ProteinsBiomarkers, TumorCell Cycle ProteinsCell ProliferationChick EmbryoGastrointestinal NeoplasmsGastrointestinal Stromal TumorsGene Expression Regulation, NeoplasticHumansNeoplasm Recurrence, LocalPrognosisSurvival RateTranscription FactorsTumor Cells, CulturedAutophagy-Related ProteinsBiomarkers, TumorCell Cycle ProteinsLix1 protein, humanTranscription FactorsYY1AP1 protein, humancancergastrointestinalLIX1sarcomasignaling pathwaysmooth muscleYAP1

Identifiers

PMID32633461
PMCPMC7417687
OpenAlexW3041478076

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.