ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
FOSL1 promotes proneural-to-mesenchymal transition of glioblastoma stem cells via UBC9/CYLD/NF-κB axis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 84 citations in OpenAlex.
- Review
- Spatial enrichment of PTPRZ1 in the peritumoral niche drives glioblastoma migration via the OPA1/ROS/CDH2 axis.Journal of translational medicine · 2026Article
- Metabolic Reprogramming in Glioblastoma Stem Cells Promotes Radiation Resistance Through a H3K18la/USP30/MBOAT2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting FOSL1-KCa3.1 inhibits ferroptosis and cartilage destruction by suppressing mitochondrial hyperfusion.Acta pharmacologica Sinica · 2026Article
- Integrative Single-Cell and Spatial Transcriptomic Analyses Link Arachidonic Acid Metabolic Reprogramming to Proneural-to-Mesenchymal State Transition in Glioblastoma.Biomedicines · 2026Article
- The role of e3 ubiquitin ligases and deubiquitinating enzymes in hepatocellular carcinoma.Cell biology and toxicology · 2026Review
- PROK2 defines a pathogenic neutrophil subset and serves as a clinical indicator of neutrophilic inflammation in COPD.Respiratory research · 2026Article
- Bufalin Inhibits the PI3K/AKT Pathway by Targeting GTF3C4 to Impede Breast Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FOSL1 promotes homologous recombination repair and camptothecin resistance via TCOF1-mediated ribosome biogenesis in non-small cell lung cancer.Translational oncology · 2026Article
- Ribosomal modifications are associated with mesenchymal fate selection in the neural crest lineage.Nature communications · 2026Article
- Review
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- Exosomal FOSL1 From Cancer-associated Fibroblasts Drives the Progression and Pro-tumorigenic M2 Macrophage Polarization of Hepatocellular Carcinoma By Activating PLAU Transcription.Applied biochemistry and biotechnology · 2026Article
- A Single Cell Atlas of the COPD Lung Identifies Inflammatory Reprogramming in Fibroblasts.International journal of chronic obstructive pulmonary disease · 2026Article
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Identification and validation of novel inflammatory response-related diagnostic biomarkers in diabetic foot ulcers.Journal of diabetes investigation · 2026Article
- Targeting the FOSL1/IKKα positive feedback loop attenuates glioblastoma malignancyTheranostics · 2026Article
- FOSL1-PRMT1 transcriptional-epigenetic circuit promotes glioblastoma radioresistance via calcyphosine-mediated DNA repair and invasion.Molecular biomedicine · 2025Article
- The HMGB1-RAGE Axis Drives the Proneural-to-Mesenchymal Transition and Aggressiveness in Glioblastoma.International journal of molecular sciences · 2025Article
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Authors and funding
17 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proneural (PN) to mesenchymal (MES) transition (PMT) is a crucial phenotypic shift in glioblastoma stem cells (GSCs). However, the mechanisms driving this process remain poorly understood. Here, we report that Fos-like antigen 1 (FOSL1), a component of AP1 transcription factor complexes, is a key player in regulating PMT. FOSL1 is predominantly expressed in the MES subtype, but not PN subtype, of GSCs. Knocking down FOSL1 expression in MES GSCs leads to the loss of MES features and tumor-initiating ability, whereas ectopic expression of FOSL1 in PN GSCs is able to induce PMT and maintain MES features. Moreover, FOSL1 facilitates ionizing radiation (IR)-induced PMT and radioresistance of PN GSCs. Inhibition of FOSL1 enhances the anti-tumor effects of IR by preventing IR-induced PMT. Mechanistically, we find that FOSL1 promotes UBC9-dependent CYLD SUMOylation, thereby inducing K63-linked polyubiquitination of major nuclear factor κB (NF-κB) intermediaries and subsequent NF-κB activation, which results in PMT induction in GSCs. Our study underscores the importance of FOSL1 in the regulation of PMT and suggests that therapeutic targeting of FOSL1 holds promise to attenuate molecular subtype switching in patients with glioblastomas.
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