Evidence mapPaperPMID 42524459Full record

ArticleInternational journal of biological sciences2026

C3G Downregulation Enhances Stemness in Glioblastoma Cells by Promoting PKM2 Upregulation.

Mateo Cueto-Remacha, Sara Manzano, Minerva Iniesta-González, Jaime Mancebo, Paula Martin-Serna, Nerea Palao, Cristina Baquero, Andrea R López-Pastor, Cristina Peralbo-Avilés, Alvaro Gutierrez-Uzquiza and 4 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mateo Cueto-RemachaDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Sara ManzanoDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Minerva Iniesta-GonzálezDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Jaime ManceboDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Paula Martin-SernaDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Nerea PalaoDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Cristina BaqueroDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Andrea R López-PastorLaboratorio de Genética y bases moleculares de enfermedades complejas. Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), 28040 Madrid, Spain.
Cristina Peralbo-AvilésDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Alvaro Gutierrez-UzquizaDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Ángel M CuestaDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Paloma BragadoDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.
Carmen GuerreroCentro de Investigación del Cáncer, Universidad de Salamanca-CSIC, 37007 Salamanca, Spain.
Almudena PorrasDepartamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM), the most common and aggressive primary brain tumor, exhibits profound metabolic reprograming that sustains its progression and therapy resistance. Our previously published work demonstrated that C3G expression is downregulated in GBM, which enhances migration and invasion. Here, we show that C3G silencing or knockout in GBM cells reprograms glucose metabolism favoring glycolysis and lactate production through upregulation of PKM2 and LDHA. Furthermore, Seahorse metabolic profiling further revealed increased respiratory capacity and glycolysis upon C3G downregulation or depletion. Mechanistically, C3G silencing increases the levels of the splicing factor PTBP1, which forces

Indexed as

Brain NeoplasmsCarrier ProteinsGlioblastomaMembrane ProteinsNeoplastic Stem CellsThyroid HormonesAnimalsCell Line, TumorDown-RegulationGene Expression Regulation, NeoplasticGlycolysisHeterogeneous-Nuclear RibonucleoproteinsHumansMetabolic ReprogrammingPolypyrimidine Tract-Binding ProteinThyroid Hormone-Binding ProteinsCarrier ProteinsHeterogeneous-Nuclear RibonucleoproteinsMembrane ProteinsPolypyrimidine Tract-Binding ProteinPTBP1 protein, humanThyroid Hormone-Binding ProteinsThyroid HormonesC3G/RapGEF1glioblastomaPKM2stemness

Identifiers

PMID42524459
PMCPMC13412097

What Socratic 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 Socratic graph.