ArticleNature communications2017
An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.
- Meta-analysis of microarray data to identify potential signature genes and MiRNAs associated with the pathogenesis of asthma.Journal of translational medicine · 2025Pooled it
- Human pancreatic progenitor organoids define genetic and epigenetic barriers to early PDAC transformation.Developmental cell · 2026Article
- Resistance to the KRASG12D Inhibitor MRTX1133 Is Associated with Increased Sensitivity to BET Inhibition.Molecular cancer therapeutics · 2026Article
- The Protein Phosphatase Inhibitor LB100 Targets the Mesenchymal Lineage of Pancreatic Ductal Adenocarcinoma.MedComm · 2026Article
- Article
- The Role of FOSL1 in Inflammatory Bowel Disease (IBD) Pathogenesis and IBD-Associated Tumorigenesis.Biomolecules · 2026Review
- FOSL1 promotes homologous recombination repair and camptothecin resistance via TCOF1-mediated ribosome biogenesis in non-small cell lung cancer.Translational oncology · 2026Article
- Epigenetic memory of colitis promotes tumour growth.Nature · 2026Article
- A Plastic EMP1+ to LGR5+ Cell State Conversion as a Bypass to KRASG12D Pharmacologic Inhibition in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Fosl1 is a transcriptional effector ofiScience · 2025Article
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Unraveling the intricate molecular landscape and potential biomarkers in lung adenocarcinoma through integrative epigenomic and transcriptomic profiling.Scientific reports · 2025Article
- FOSL1 drives the malignant progression of pancreatic cancer cells by regulating cell stemness, metastasis and multidrug efflux system.Journal of translational medicine · 2025Article
- Single cell transcriptomic analysis reveals tumor immune infiltration by macrophage cells gene signature in lung adenocarcinoma.Discover oncology · 2025Article
- KLF14 inhibits tumor progression via FOSL1 in glioma.Biochemistry and biophysics reports · 2025Article
- Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- RNA Sequencing Identifies Novel Signaling Pathways and Potential Drug Target Genes Induced by FOSL1 in Glioma Progression and Stemness.Biologics : targets & therapy · 2025Article
- Construction of an Extracellular Matrix-Related Risk Model to Analyze the Correlation Between Glioblastoma and Tumor Immunity.BioMed research international · 2025Article
- FRA1 controls acinar cell plasticity during murine KrasDevelopmental cell · 2024Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 9 institutions in 7 countries.
Funding
Abstract
KRAS mutated tumours represent a large fraction of human cancers, but the vast majority remains refractory to current clinical therapies. Thus, a deeper understanding of the molecular mechanisms triggered by KRAS oncogene may yield alternative therapeutic strategies. Here we report the identification of a common transcriptional signature across mutant KRAS cancers of distinct tissue origin that includes the transcription factor FOSL1. High FOSL1 expression identifies mutant KRAS lung and pancreatic cancer patients with the worst survival outcome. Furthermore, FOSL1 genetic inhibition is detrimental to both KRAS-driven tumour types. Mechanistically, FOSL1 links the KRAS oncogene to components of the mitotic machinery, a pathway previously postulated to function orthogonally to oncogenic KRAS. FOSL1 targets include AURKA, whose inhibition impairs viability of mutant KRAS cells. Lastly, combination of AURKA and MEK inhibitors induces a deleterious effect on mutant KRAS cells. Our findings unveil KRAS downstream effectors that provide opportunities to treat KRAS-driven cancers.
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Registered trials
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.