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FRA1 (FOSL1) Suppresses Neoplastic Transformation and Modulates Radiation Responses via Transcriptional Control of Mitogenic and Stress-Responsive Networks

GSE307991 Homo sapiens (human) RNA-seq (gene expression) 22 samples Submitted 2025/09/15 Platform GPL34281
At a glance

RNA-seq (gene expression) · human · 22 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
22 samples: 8 conditions, mostly in triplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
FRA1 (FOSL1) suppresses neoplastic transformation and modulates radiation responses via transcriptional control of mitogenic and stress-responsive networksFrontiers in cell and developmental biology · 2025
Summary (written by the submitters)
Purpose: FOS-like antigen 1 (FRA1), encoded by FOSL1, is an inducible subunit of the AP-1 transcription factor complex and regulates gene expression in response to proliferative and environmental cues. Although FRA1 has been linked to cancer progression, its role in early transformation and radiation responses remains unclear. 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.
Read the full summary ↓
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.
Published in
FRA1 (FOSL1) suppresses neoplastic transformation and modulates radiation responses via transcriptional control of mitogenic and stress-responsive networks
Al-Khayyat W, Laframboise T, Dougherty J et al. · Frontiers in cell and developmental biology 2025 · PMID 41059335 · doi:10.3389/fcell.2025.1659986
This dataset
Open GSE307991 in finder → Find more human RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE307991_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1327934 and SRA study SRP619866. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41059335) ↗
Study design
8 conditions, mostly in triplicate
WA_Cas9 0hr _Serum Stimulation ×3 WA_KO 0hr _Serum Stimulation ×3 WA_FRA1 0hrs_Serum Stimulation ×3 WA_Cas9 2hrs_Serum Stimulation ×3 WA_KO 2hrs_Serum Stimulation ×3 WA_dCas9 2hrs _Serum Stimulation ×3 WA_dCas9 0hrs _Serum Stimulation ×2 WA_FRA1 2hrs _Serum Stimulation ×2

Supports a between-group comparison across 22 samples.

How we read this: 8 replicated groups read from 22 sample titles; they account for 22 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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