Evidence map›Paper›PMID 27002148›Full record

ArticleThe Journal of biological chemistry2016

A Positive Feed-forward Loop Associating EGR1 and PDGFA Promotes Proliferation and Self-renewal in Glioblastoma Stem Cells.

Nathalie Sakakini, Laurent Turchi, Aurélie Bergon, Hélène Holota, Samah Rekima, Fabrice Lopez, Philipe Paquis, Fabien Almairac, Denys Fontaine, Nathalie Baeza-Kallee and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 44 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

17 authors at 8 institutions in 1 country.

Nathalie SakakiniFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France, INSERM, U1090, Transcriptomic and Genomic Marseille-Luminy/Technical Advances for Genomics and Clinics (TGML/TAGC), Marseille F-13009, France, UMR_S 1090, TGML/TAGC, Aix-Marseille Université, Marseille F-13009, France.
Laurent TurchiFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France.
Aurélie BergonINSERM, U1090, Transcriptomic and Genomic Marseille-Luminy/Technical Advances for Genomics and Clinics (TGML/TAGC), Marseille F-13009, France, UMR_S 1090, TGML/TAGC, Aix-Marseille Université, Marseille F-13009, France.
Hélène HolotaINSERM, U1090, Transcriptomic and Genomic Marseille-Luminy/Technical Advances for Genomics and Clinics (TGML/TAGC), Marseille F-13009, France, UMR_S 1090, TGML/TAGC, Aix-Marseille Université, Marseille F-13009, France.
Samah RekimaFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France.
Fabrice LopezINSERM, U1090, Transcriptomic and Genomic Marseille-Luminy/Technical Advances for Genomics and Clinics (TGML/TAGC), Marseille F-13009, France, UMR_S 1090, TGML/TAGC, Aix-Marseille Université, Marseille F-13009, France.
Philipe PaquisFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France, the Service de Neurchirurgie, Hôpital Pasteur, CHU de Nice, Nice 06107, France.
Fabien AlmairacFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France, the Service de Neurchirurgie, Hôpital Pasteur, CHU de Nice, Nice 06107, France.
Denys Fontainethe Service de Neurchirurgie, Hôpital Pasteur, CHU de Nice, Nice 06107, France.
Nathalie Baeza-KalleeAix Marseille Université, Faculté de Médecine de la Timone, 13284 Marseille, France, CRO2, INSERM UMR 911, 13284 Marseille Cedex, France.
Ellen Van Obberghen-SchillingFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France.
Marie-Pierre JunierCNRS UMR8246 Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France, INSERM U1130, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France, and University Pierre and Marie Curie UMCR18, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France.
Hervé ChneiweissCNRS UMR8246 Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France, INSERM U1130, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France, and University Pierre and Marie Curie UMCR18, Neuroscience Paris Seine-IBPS, Team Glial Plasticity, 7 Quai Saint-Bernard, Paris 75005, France.
Dominique Figarella-BrangerAix Marseille Université, Faculté de Médecine de la Timone, 13284 Marseille, France, CRO2, INSERM UMR 911, 13284 Marseille Cedex, France, the Departement de Pathology, CHU de la Timone, 13385 Marseille Cedex 5, France.
Fanny Burel-VandenbosFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France, the Service d'Anatomopathologie, Hôpital Pasteur, CHU de Nice, Nice 06107, France.
Jean ImbertINSERM, U1090, Transcriptomic and Genomic Marseille-Luminy/Technical Advances for Genomics and Clinics (TGML/TAGC), Marseille F-13009, France, UMR_S 1090, TGML/TAGC, Aix-Marseille Université, Marseille F-13009, France, jean.imbert@inserm.fr.
Thierry VirolleFrom the Université Nice Sophia Antipolis, CNRS, INSERM, iBV, 06108 Nice, France, virolle@unice.fr.
Inserm · FRCentre National de la Recherche Scientifique · FRUniversité Côte d'Azur · FRAix-Marseille Université · FRCentre Hospitalier Universitaire de Nice · FRHôpital de la Timone · FRHôpital Pasteur · FRTheories and Approaches of Genomic Complexity · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas are the most common primary brain tumors, highly vascularized, infiltrating, and resistant to current therapies. This cancer leads to a fatal outcome in less than 18 months. The aggressive behavior of glioblastomas, including resistance to current treatments and tumor recurrence, has been attributed to glioma stemlike/progenitor cells. The transcription factor EGR1 (early growth response 1), a member of a zinc finger transcription factor family, has been described as tumor suppressor in gliomas when ectopically overexpressed. Although EGR1 expression in human glioblastomas has been associated with patient survival, its precise location in tumor territories as well as its contribution to glioblastoma progression remain elusive. In the present study, we show that EGR1-expressing cells are more frequent in high grade gliomas where the nuclear expression of EGR1 is restricted to proliferating/progenitor cells. We show in primary cultures of glioma stemlike cells that EGR1 contributes to stemness marker expression and proliferation by orchestrating a PDGFA-dependent growth-stimulatory loop. In addition, we demonstrate that EGR1 acts as a positive regulator of several important genes, including SHH, GLI1, GLI2, and PDGFA, previously linked to the maintenance and proliferation of glioma stemlike cells.

Indexed as

Autocrine CommunicationCell ProliferationGene Expression Regulation, NeoplasticBrain NeoplasmsEarly Growth Response Protein 1FemaleGlioblastomaHumansMaleNeoplasm ProteinsNeoplastic Stem CellsPlatelet-Derived Growth FactorTumor Cells, CulturedEarly Growth Response Protein 1EGR1 protein, humanNeoplasm ProteinsPlatelet-Derived Growth Factorplatelet-derived growth factor Acancer biologycancer stem cellscell proliferationcell signalingtranscription factor

Identifiers

PMID27002148
PMCPMC4865916
OpenAlexW2334436911

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.