ReviewJournal of experimental & clinical cancer research : CR2020
Selective antagonism of cJun for cancer therapy.
Review in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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.
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.
Who cites it
55 citing papers in PubMed, 93 citations in OpenAlex.
- Glucose-induced histone lactylation confers metformin resistance in colorectal cancer stem cells.Nature communications · 2026Article
- Lactate-associated H3K18la upregulates RNF166 to promote immune evasion in hepatocellular carcinoma by remodeling c-Jun ubiquitination.Apoptosis : an international journal on programmed cell death · 2026Article
- SF1 regulates the transcription of FDX1 to promote cuproptosis in pediatric sepsis-related acute lung injury by interacting with cJUN.Biology direct · 2026Article
- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- Novel pyridine-based chalcone analogs and triple negative breast cancer: potential therapy & molecular pathways.Scientific reports · 2026Article
- Efficient In Vivo Pharmacological Inhibition of ΔFOSB, an AP-1 Transcription Factor, in the Brain.ACS chemical neuroscience · 2026Article
- InsiliCoil: An Integrated Software Suite for Coiled Coil Design, Prediction, and Therapeutic Engineering.ACS synthetic biology · 2026Article
- Identification of Bioactive Compounds and Molecular Targets of Compound Herbs Against Stomach Adenocarcinoma: A Network Pharmacology Approach.International journal of general medicine · 2026Article
- c-Jun inhibition mitigates chemotherapy-induced neurotoxicity in iPSC-derived sensory neurons.Cell death discovery · 2025Article
- Synergistic roles of NFATc1 and c-Jun in immunomodulation.Biochemistry and biophysics reports · 2025Review
- Integrative multi-omics identifies AP-1 transcription factor as a targetable mediator of acquired osimertinib resistance in non-small cell lung cancer.Cell death & disease · 2025Article
- An Intracellular Peptide Library Screening Platform Identifies Irreversible Covalent Transcription Factor Inhibitors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- Protective role of triiodothyronine in sepsis‑induced cardiomyopathy through phospholamban downregulation.International journal of molecular medicine · 2025Article
- Mitoregulin Promotes Cell Cycle Progression in Non-Small Cell Lung Cancer Cells.International journal of molecular sciences · 2025Article
- Jun, an Oncological Foe or Friend?International journal of molecular sciences · 2025Review
- Impact of c-JUN deficiency on thalamus development in mice and human neural models.Cell & bioscience · 2024Article
- Two-polarized roles of transcription factor FOSB in lung cancer progression and prognosis: dependent on p53 status.Journal of experimental & clinical cancer research : CR · 2024Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The activator protein-1 (AP-1) family of transcription factors modulate a diverse range of cellular signalling pathways into outputs which can be oncogenic or anti-oncogenic. The transcription of relevant genes is controlled by the cellular context, and in particular by the dimeric composition of AP-1. Here, we describe the evidence linking cJun in particular to a range of cancers. This includes correlative studies of protein levels in patient tumour samples and mechanistic understanding of the role of cJun in cancer cell models. This develops an understanding of cJun as a focal point of cancer-altered signalling which has the potential for therapeutic antagonism. Significant work has produced a range of small molecules and peptides which have been summarised here and categorised according to the binding surface they target within the cJun-DNA complex. We highlight the importance of selectively targeting a single AP-1 family member to antagonise known oncogenic function and avoid antagonism of anti-oncogenic function.
Indexed as
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What OpenQuestion holds
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.