Evidence map›Paper›PMID 41059335›Full record

ArticleFrontiers in cell and developmental biology2025

FRA1 (

Wuroud Al-Khayyat, Taylor Laframboise, Jessica Dougherty, Marc S Mendonca, Douglas R Boreham, T C Tai, Christopher Thome, Sujeenthar Tharmalingam

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Wuroud Al-KhayyatBiomolecular Sciences Program, School of Natural Sciences, Laurentian University, Sudbury, ON, Canada.
Taylor LaframboiseMedical Sciences Division, NOSM University, Sudbury, ON, Canada.
Jessica DoughertyMedical Sciences Division, NOSM University, Sudbury, ON, Canada.
Marc S MendoncaRadiation and Cancer Biology Laboratories, Department of Radiation Oncology, and Department of Medical & Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, United States.
Douglas R BorehamBiomolecular Sciences Program, School of Natural Sciences, Laurentian University, Sudbury, ON, Canada.
T C TaiBiomolecular Sciences Program, School of Natural Sciences, Laurentian University, Sudbury, ON, Canada.
Christopher ThomeBiomolecular Sciences Program, School of Natural Sciences, Laurentian University, Sudbury, ON, Canada.
Sujeenthar TharmalingamBiomolecular Sciences Program, School of Natural Sciences, Laurentian University, Sudbury, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: FOS-like antigen 1 (FRA1), encoded by Methods: CRISPR-engineered human CGL1 cells-a hybrid of HeLa and normal fibroblasts-were used to evaluate the impact of FRA1 overexpression and knockout on neoplastic transformation. Transformation frequency, clonogenic survival, DNA damage recognition and repair, and cell cycle distribution were assessed following irradiation. Transcriptomic profiling was performed under baseline and serum-stimulated conditions. Results: FRA1 loss markedly increased both spontaneous and radiation-induced transformation frequency, while overexpression suppressed transformation under both conditions. FRA1-deficient cells were sensitized to radiation-induced cell killing, despite intact DNA damage recognition and repair. In contrast, FRA1 overexpression promoted G2/M accumulation post-irradiation, suggesting enhanced checkpoint activation. Transcriptomic profiling revealed that FRA1 remodels AP-1 complex composition and functions as a transcriptional repressor of mitogen- and stress-responsive genes. FRA1-mediated repression was observed across gene networks involved in extracellular matrix remodeling, hypoxia signaling, inflammation, and proliferation, under both baseline and serum-stimulated conditions. Conclusion: These findings establish FRA1 as a key modulator of neoplastic transformation and radiation response, acting primarily through transcriptional repression of pro-tumorigenic signaling pathways.

Indexed as

AP-1 transcription factorCGL1 hybrid cell lineCRISPRFOSL1FRA1gene expressionneoplastic transformationradiation-induced carcinogenesis

Identifiers

PMID41059335
PMCPMC12497744

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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.