ArticleCell death and differentiation2015
Loss of JUNB/AP-1 promotes invasive prostate cancer.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Macrophage-derived CTSZ promotes prostate cancer progression via αVβ3 integrin-mediated activation of the AKT/FOXO1/JUNB signaling axis.Cancer cell international · 2026Article
- A unique transcriptomic landscape defines African-specific grade group 1 prostate cancer.Research square · 2026Article
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- Evaluation of potential prognostic significance of JUNB in human prostate cancer: a bioinformatic and histopathological study.Journal of pathology and translational medicine · 2025Article
- JUNB O-GlcNAcylation-Mediated Promoter Accessibility of Metabolic Genes Modulates Distinct Epithelial Lineage in Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Spatial tumor immune heterogeneity facilitates subtype co-existence and therapy response in pancreatic cancer.Nature communications · 2025Article
- A new effLuc/Kate dual reporter allele for tumor imaging in mice.Disease models & mechanisms · 2025Article
- Current landscape of exosomal non-coding RNAs in prostate cancer: Modulators and biomarkers.Non-coding RNA research · 2024Review
- Single-cell data revealed the regulatory mechanism of TNK cell heterogeneity in liver metastasis from gastric cancer.Discover oncology · 2024Article
- Article
- JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.Molecular cancer · 2024Article
- Review
- The androgen receptor interacts with GATA3 to transcriptionally regulate a luminal epithelial cell phenotype in breast cancer.Genome biology · 2024Article
- Discovery of neddylation E2s inhibitors with therapeutic activity.Oncogenesis · 2023Review
- Pre-Clinical Models to Study Human Prostate Cancer.Cancers · 2023Review
- Conserved transcription factors promote cell fate stability and restrict reprogramming potential in differentiated cells.Nature communications · 2023Article
- Post-prostatic-massage urine exosomes of men with chronic prostatitis/chronic pelvic pain syndrome carry prostate-cancer-typical microRNAs and activate proto-oncogenes.Molecular oncology · 2023Article
- Lysyl oxidase-like 4 exerts an atypical role in breast cancer progression that is dependent on the enzymatic activity that targets the cell-surface annexin A2.Frontiers in oncology · 2023Article
- JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023Review
- Differential regulation of TNFα and IL-6 expression contributes to immune evasion in prostate cancer.Journal of translational medicine · 2022Article
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6 authors at 1 institution in 1 country.
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Abstract
Prostate cancer is a frequent cause of male death in the Western world. Relatively few genetic alterations have been identified, likely owing to disease heterogeneity. Here, we show that the transcription factor JUNB/AP-1 limits prostate cancer progression. JUNB expression is increased in low-grade prostate cancer compared with normal human prostate, but downregulated in high-grade samples and further decreased in all metastatic samples. To model the hypothesis that this downregulation is functionally significant, we genetically inactivated Junb in the prostate epithelium of mice. When combined with Pten (phosphatase and tensin homologue) loss, double-mutant mice were prone to invasive cancer development. Importantly, invasive tumours also developed when Junb and Pten were inactivated in a small cell population of the adult anterior prostate by topical Cre recombinase delivery. The resulting tumours displayed strong histological similarity with human prostate cancer. Loss of JunB expression led to increased proliferation and decreased senescence, likely owing to decreased p16(Ink4a) and p21(CIP1) in epithelial cells. Furthermore, the tumour stroma was altered with increased osteopontin and S100 calcium-binding protein A8/9 expression, which correlated with poor prognoses in patients. These data demonstrate that JUNB/AP-1 cooperates with PTEN signalling as barriers to invasive prostate cancer, whose concomitant genetic or epigenetic suppression induce malignant progression.
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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.