Evidence map›Paper›PMID 27641066›Full record

ArticleJournal of cellular and molecular medicine2017

KLRC3, a Natural Killer receptor gene, is a key factor involved in glioblastoma tumourigenesis and aggressiveness.

Mathilde Cheray, Barbara Bessette, Aurélie Lacroix, Carole Mélin, Soha Jawhari, Sandra Pinet, Elise Deluche, Pierre Clavère, Karine Durand, Ricardo Sanchez-Prieto and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. 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
0.6field-weighted citation impact, top 30% 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, 24 citations in OpenAlex.

  1. Article
  2. NKG2C/Journal for immunotherapy of cancer · 2024
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  7. Review
  8. Advances in NK cell therapy for brain tumors.NPJ precision oncology · 2023
    Review
  9. Article
  10. Article
  11. Article
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  13. Review
  14. Review
  15. Identification ofFrontiers in oncology · 2020
    Article
  16. Article
  17. Article
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

13 authors at 2 institutions in 2 countries.

Mathilde CherayEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Barbara BessetteEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Aurélie LacroixEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Carole MélinEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Soha JawhariEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Sandra PinetEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Elise DelucheOncology Department, University Hospital, Limoges, France.
Pierre ClavèreEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Karine DurandEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Ricardo Sanchez-PrietoLaboratorio de Oncología Molecular, Centro Regional de Investigaciones Biomédicas, Universidad de Castilla-La Mancha/PCyTA/Unidad de Biomédicina UCLM-CSIC, Albacete, Spain.
Marie-Odile JauberteauEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Serge BattuEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Fabrice LallouéEA3842 Homéostasie Cellulaire et Pathologies, Faculty of Medicine of Limoges, University of Limoges, Limoges, France.
Université de Limoges · FRUniversity of Castilla-La Mancha · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most lethal brain tumour with a poor prognosis. Cancer stem cells (CSC) were proposed to be the most aggressive cells allowing brain tumour recurrence and aggressiveness. Current challenge is to determine CSC signature to characterize these cells and to develop new therapeutics. In a previous work, we achieved a screening of glycosylation-related genes to characterize specific genes involved in CSC maintenance. Three genes named CHI3L1, KLRC3 and PRUNE2 were found overexpressed in glioblastoma undifferentiated cells (related to CSC) compared to the differentiated ones. The comparison of their roles suggest that KLRC3 gene coding for NKG2E, a protein initially identified in NK cells, is more important than both two other genes in glioblastomas aggressiveness. Indeed, KLRC3 silencing decreased self-renewal capacity, invasion, proliferation, radioresistance and tumourigenicity of U87-MG glioblastoma cell line. For the first time we report that KLRC3 gene expression is linked to glioblastoma aggressiveness and could be a new potential therapeutic target to attenuate glioblastoma.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisBrain NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationClone CellsFemaleGene Expression Regulation, NeoplasticGene SilencingGlioblastomaGlycogen Synthase Kinase 3 betaHumansMembrane ProteinsAdaptor Proteins, Signal TransducingGlycogen Synthase Kinase 3 betaKLRC3 protein, humanMembrane ProteinsNK Cell Lectin-Like Receptor Subfamily CRNA, Small InterferingTYROBP protein, humanbiomarkerglioblastomaNKG2E/KLRC3tumourigenicity

Identifiers

PMID27641066
PMCPMC5264145
OpenAlexW2522566065

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.