Evidence map›Paper›PMID 29948952›Full record

ArticleMolecular neurobiology2019

GBM-Derived Wnt3a Induces M2-Like Phenotype in Microglial Cells Through Wnt/β-Catenin Signaling.

Diana Matias, Luiz Gustavo Dubois, Bruno Pontes, Luciane Rosário, Valeria Pereira Ferrer, Joana Balça-Silva, Anna Carolina Carvalho Fonseca, Lucy Wanjiku Macharia, Luciana Romão, Tania Cristina Leite de Sampaio E Spohr and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  6. Immunotherapy in central nervous system tumors.International journal of surgery (London, England) · 2025
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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

16 authors at 4 institutions in 2 countries.

Diana MatiasLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Luiz Gustavo DuboisLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Bruno PontesInstituto de Ciências Biomédicas da Universidade Federal do Rio de Janeiro (ICB/UFRJ), Rio de Janeiro, 21941-902, Brazil.
Luciane RosárioLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Valeria Pereira FerrerLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Joana Balça-SilvaLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Anna Carolina Carvalho FonsecaInstituto de Ciências Biomédicas da Universidade Federal do Rio de Janeiro (ICB/UFRJ), Rio de Janeiro, 21941-902, Brazil.
Lucy Wanjiku MachariaLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Luciana RomãoInstituto de Ciências Biomédicas da Universidade Federal do Rio de Janeiro (ICB/UFRJ), Rio de Janeiro, 21941-902, Brazil.
Tania Cristina Leite de Sampaio E SpohrLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Leila ChimelliLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Paulo Niemeyer FilhoLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil.
Maria Celeste LopesCentro de Neurociências e Biologia celular e Instituto Biomédico da Imagem e das Ciências da Vida (CNC.IBILI), Coimbra, Portugal.
José Garcia AbreuInstituto de Ciências Biomédicas da Universidade Federal do Rio de Janeiro (ICB/UFRJ), Rio de Janeiro, 21941-902, Brazil.
Flavia Regina Souza LimaInstituto de Ciências Biomédicas da Universidade Federal do Rio de Janeiro (ICB/UFRJ), Rio de Janeiro, 21941-902, Brazil.
Vivaldo Moura-NetoLaboratório de Biomedicina do Cérebro, Instituto Estadual do Cérebro Paulo Niemeyer, Secretaria de Saúde do Estado do Rio de Janeiro, Rua do Resende 156, Rio de Janeiro, CEP 20231-092, Brazil. vivaldomouraneto@gmail.com.ORCID http://orcid.org/0000-0003-0303-1868
Universidade Federal do Rio de Janeiro · BRInstituto Estadual do Cérebro Paulo Niemeyer · BRAssociation for Innovation and Biomedical Research on Light and Image · PTHospitais da Universidade de Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is an extremely aggressive and deadly brain tumor known for its striking cellular heterogeneity and capability to communicate with microenvironment components, such as microglia. Microglia-glioblastoma interaction contributes to an increase in tumor invasiveness, and Wnt signaling pathway is one of the main cascades related to tumor progression through changes in cell migration and invasion. However, very little is known about the role of canonical Wnt signaling during microglia-glioblastoma crosstalk. Here, we show for the first time that Wnt3a is one of the factors that regulate interactions between microglia and glioblastoma cells. Wnt3a activates the Wnt/β-catenin signaling of both glioblastoma and microglial cells. Glioblastoma-conditioned medium not only induces nuclear translocation of microglial β-catenin but also increases microglia viability and proliferation as well as Wnt3a, cyclin-D1, and c-myc expression. Moreover, glioblastoma-derived Wnt3a increases microglial ARG-1 and STI1 expression, followed by an upregulation of IL-10 mRNA levels, and a decrease in IL1β gene expression. The presence of Wnt3a in microglia-glioblastoma co-cultures increases the formation of membrane nanotubes accompanied by changes in migration capability. In vivo, tumors formed from Wnt3a-stimulated glioblastoma cells presented greater microglial infiltration and more aggressive characteristics such as growth rate than untreated tumors. Thus, we propose that Wnt3a belongs to the arsenal of factors capable of stimulating the induction of M2-like phenotype on microglial cells, which contributes to the poor prognostic of glioblastoma, reinforcing that Wnt/β-catenin pathway can be a potential therapeutic target to attenuate glioblastoma progression.

Indexed as

beta CateninCell MovementCell ProliferationGlioblastomaHumansMicrogliaPhenotypeWnt3A ProteinWnt Signaling Pathwaybeta CateninCTNNB1 protein, humanWnt3A ProteinWNT3A protein, humanGlioblastomaM2-like phenotypeMicrogliaWnt3aWnt/β-catenin pathway

Identifiers

PMID29948952
OpenAlexW2808235471

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.