Evidence map›Paper›PMID 42113357›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

Elevated GCN2 levels in cancer cells confer protection from mitotic stress and faster cell movement.

Vilte Stonyte, Christina Saeten Fjeldbo, Mélanie Langiu, Michelle Joy-Immediato, Priyanka Swaminathan, Prabin Sharma Humagain, Laura Marian Valencia-Pesqueira, Lilian Lindbergsengen, Coen Campsteijn, Heidi Lyng and 1 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

11 authors.

Vilte StonyteDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Christina Saeten FjeldboDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Mélanie LangiuDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Michelle Joy-ImmediatoInstitute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
Priyanka SwaminathanDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Prabin Sharma HumagainDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Laura Marian Valencia-PesqueiraDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Lilian LindbergsengenDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Coen CampsteijnInstitute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Oslo, Norway.
Heidi LyngDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Beata GrallertDepartment of Radiation Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway. beata@ous-hf.no.ORCID http://orcid.org/0000-0001-5917-0555

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHigh expression of the stress-response kinase GCN2 has been linked to poor survival in several cancers including cervical cancer, but its underlying biological roles remain incompletely understood. This study aimed to identify genes whose expression correlates with GCN2 in locally advanced cervical cancer and to use these associations to elucidate cellular functions that could contribute to aggressive disease behavior.

methodsCorrelation analyses were performed between GCN2 expression and genome-wide mRNA profiles in a biobank of 291 patients with locally advanced cervical cancer. Gene ontology and pathway analyses were used to identify enriched biological processes, and functional assays were conducted to validate GCN2 involvement in selected pathways.

resultsGCN2 expression correlated not only with genes involved in cellular stress responses but also with those regulating mitosis and cell migration. Functional analyses confirmed that GCN2 activity promotes both proliferative and migratory capacities, revealing important cancer-relevant roles beyond its canonical function in translational control.

conclusionOur findings demonstrate that elevated GCN2 levels support cellular functions that can contribute to tumor aggressiveness. These results suggest that GCN2 plays a direct role in malignant progression and may represent a potential biomarker or therapeutic target in locally advanced cervical cancer.

Indexed as

Cell MovementMitosisProtein Serine-Threonine KinasesStress, PhysiologicalUterine Cervical NeoplasmsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansRNA, MessengerEIF2AK4 protein, humanProtein Serine-Threonine KinasesRNA, MessengerCell migrationCytoskeletal dynamicsGCN2Mitotic stressPP1

Identifiers

PMID42113357
PMCPMC13346413

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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.