Evidence map›Paper›PMID 32218467›Full record

ArticleScientific reports2020

Transformation Foci in IDH1-mutated Gliomas Show STAT3 Phosphorylation and Downregulate the Metabolic Enzyme ETNPPL, a Negative Regulator of Glioma Growth.

N Leventoux, M Augustus, S Azar, S Riquier, J P Villemin, S Guelfi, L Falha, L Bauchet, C Gozé, W Ritchie and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
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  6. Glial Cell Adhesion Molecule (GlialCAM) Determines Proliferative versus Invasive Cell States in Glioblastoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  7. The prognostic value of DAAM2 in lower grade glioma, liver cancer, and breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  8. Review
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  14. 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

14 authors.

N LeventouxInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.ORCID http://orcid.org/0000-0001-7023-9859
M AugustusInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
S AzarInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
S RiquierInstitute for Regenerative Medicine & Biotherapy, Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
J P VilleminInstitute of Human Genetics, Centre National de la Recherche Scientifique (CNRS). UMR9002, 141 rue de la Cardonille, 34000, Montpellier, France.
S GuelfiInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
L FalhaInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
L BauchetInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
C GozéInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
W RitchieInstitute of Human Genetics, Centre National de la Recherche Scientifique (CNRS). UMR9002, 141 rue de la Cardonille, 34000, Montpellier, France.ORCID http://orcid.org/0000-0001-8162-1439
T CommesInstitute for Regenerative Medicine & Biotherapy, Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.
H DuffauInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.ORCID http://orcid.org/0000-0002-6558-2342
V RigauInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France.ORCID http://orcid.org/0000-0002-8017-5489
J P HugnotInstitute for Neurosciences of Montpellier, Institut National de la Santé et de la Recherche Médicale (INSERM). U1051 - Hôpital Saint-Éloi, 80 Avenue Augustin Fliche - 34091 Montpellier cedex 5, Montpellier, France. jean-philippe.hugnot@umontpellier.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IDH1-mutated gliomas are slow-growing brain tumours which progress into high-grade gliomas. The early molecular events causing this progression are ill-defined. Previous studies revealed that 20% of these tumours already have transformation foci. These foci offer opportunities to better understand malignant progression. We used immunohistochemistry and high throughput RNA profiling to characterize foci cells. These have higher pSTAT3 staining revealing activation of JAK/STAT signaling. They downregulate RNAs involved in Wnt signaling (DAAM2, SFRP2), EGFR signaling (MLC1), cytoskeleton and cell-cell communication (EZR, GJA1). In addition, foci cells show reduced levels of RNA coding for Ethanolamine-Phosphate Phospho-Lyase (ETNPPL/AGXT2L1), a lipid metabolism enzyme. ETNPPL is involved in the catabolism of phosphoethanolamine implicated in membrane synthesis. We detected ETNPPL protein in glioma cells as well as in astrocytes in the human brain. Its nuclear localization suggests additional roles for this enzyme. ETNPPL expression is inversely correlated to glioma grade and we found no ETNPPL protein in glioblastomas. Overexpression of ETNPPL reduces the growth of glioma stem cells indicating that this enzyme opposes gliomagenesis. Collectively, these results suggest that a combined alteration in membrane lipid metabolism and STAT3 pathway promotes IDH1-mutated glioma malignant progression.

Indexed as

Brain NeoplasmsCarbon-Oxygen LyasesCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease ProgressionDown-RegulationGene Expression ProfilingGliomaHumansImmunohistochemistryIsocitrate DehydrogenaseLipid MetabolismMutationPhosphorylationSignal TransductionCarbon-Oxygen Lyasesethanolaminephosphate phospho-lyaseIDH1 protein, humanIsocitrate DehydrogenaseSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID32218467
PMCPMC7099072

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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.