ArticleNature communications2015
STAT3 regulated ARF expression suppresses prostate cancer metastasis.
Erratum issuedOpen access · goldAbstract read
In one paragraph
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 101 papers, 2 of them syntheses that pooled it.
0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 2 pooled it
9.5field-weighted citation impact, top 1% of its field
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Who cites it
101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- Efficacy of Using Dendritic Cells in the Treatment of Prostate Cancer: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- BioBERT-powered synergy: advanced bibliometric and molecular insights into prostate cancer bone metastasis.Frontiers in immunology · 2025Pooled it
- Synthesis and application of exopolysaccharide-selenium nanocomposite produced by Pseudoduganella armeniaca ZMN-3.BMC biotechnology · 2026Article
- Biobank of genetically defined murine prostate cancer tumoroids uncovers oncogenic pathways and drug vulnerabilities driven by PTEN-loss.Cell reports methods · 2026Article
- Mechanistic insights and molecular therapy for neuroendocrine prostate cancer.Frontiers in oncology · 2026Review
- Nuclear STAT3 expression is associated with favorable prognosis in papillary thyroid carcinoma.European thyroid journal · 2025Article
- Cellular senescence offers distinct immunological vulnerabilities in cancer.Trends in cancer · 2025Review
- p53-loss induced prostatic epithelial cell plasticity and invasion is driven by a crosstalk with the tumor microenvironment.Cell death & disease · 2025Article
- Cell-autonomous IL6ST activation suppresses prostate cancer development via STAT3/ARF/p53-driven senescence and confers an immune-active tumor microenvironment.Molecular cancer · 2024Article
- JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.Molecular cancer · 2024Article
- NRN1 interacts with Notch to increase oncogenic STAT3 signaling in melanoma.Cell communication and signaling : CCS · 2024Article
- Exploring Novel Frontiers: Leveraging STAT3 Signaling for Advanced Cancer Therapeutics.Cancers · 2024Review
- A novel assessment of whole-mount Gleason grading in prostate cancer to identify candidates for radical prostatectomy: a machine learning-based multiomics study.Theranostics · 2024Article
- Pre-Clinical Models to Study Human Prostate Cancer.Cancers · 2023Review
- STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway.Molecular cancer · 2023Article
- Exploring the Onset and Progression of Prostate Cancer through a Multicellular Agent-based Model.Cancer research communications · 2023Article
- JAKs and STATs from a Clinical Perspective: Loss-of-Function Mutations, Gain-of-Function Mutations, and Their Multidimensional Consequences.Journal of clinical immunology · 2023Review
- A Review of Gut Microbiota-Derived Metabolites in Tumor Progression and Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Tissue-specific biological aging predicts progression in prostate cancer and acute myeloid leukemia.Frontiers in oncology · 2023Article
- A new approach: Evaluation of necroptosis and immune status enables prediction of the tumor microenvironment and treatment targets in pancreatic cancer.Computational and structural biotechnology journal · 2023Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Erratum issued
Authors and funding
40 authors at 16 institutions in 6 countries.
Jan Pencik1] Ludwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria. [2] Clinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Michaela Schlederer1] Ludwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria [2] Clinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Wolfgang GruberDepartment of Molecular Biology, Paris-Lodron University of Salzburg, 5020 Salzburg, Austria.
Christine UngerInstitute of Medical Genetics, Medical University of Vienna, 1090 Vienna, Austria.
Steven M WalkerCenter for Cancer Research and Cell Biology, Queen's University Belfast, BT7 1NN Belfast, UK.
Athena ChalarisInstitute of Biochemistry, University of Kiel, 24098 Kiel, Germany.
Isabelle J Marié1] Department of Pathology and NYU Cancer Institute, NYU School of Medicine, New York 10016, USA [2] Department of Microbiology and NYU Cancer Institute, NYU School of Medicine, New York 10016, USA.
Melanie R HasslerClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Tahereh JavaheriLudwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria.
Osman AksoyClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Jaine K BlayneyNI Stratified Medicine Research Group, University of Ulster, BT47 6SB Londonderry, UK.
Nicole PrutschClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Anna SkuchaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria.
Merima HeracClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Oliver H KrämerDepartment of Toxicology, University Medical Center, 55131 Mainz, Germany.
Peter MazalClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Florian GrebienLudwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria.
Gerda EggerClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Valeria PoliMolecular Biotechnology Center (MBC), Department of Genetics, Biology and Biochemistry, University of Turin, Turin 10126, Italy.
Wolfgang MikulitsDepartment of Medicine I, Division: Institute for Cancer Research, Comprehensive Cancer Center, Medical University of Vienna, 1090 Vienna, Austria.
Robert EferlDepartment of Medicine I, Division: Institute for Cancer Research, Comprehensive Cancer Center, Medical University of Vienna, 1090 Vienna, Austria.
Harald EsterbauerDepartment of Laboratory Medicine, Medical University of Vienna, 1090 Vienna, Austria.
Richard KennedyCenter for Cancer Research and Cell Biology, Queen's University Belfast, BT7 1NN Belfast, UK.
Falko FendInstitute of Pathology and Neuropathology, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Marcus ScharpfInstitute of Pathology and Neuropathology, University Hospital Tuebingen, 72076 Tuebingen, Germany.
Martin BraunInstitute of Pathology, Center for Integrated Oncology Cologne/Bonn, University Hospital of Bonn, 53127 Bonn, Germany.
Sven PernerInstitute of Pathology, Center for Integrated Oncology Cologne/Bonn, University Hospital of Bonn, 53127 Bonn, Germany.
David E Levy1] Department of Pathology and NYU Cancer Institute, NYU School of Medicine, New York 10016, USA [2] Department of Microbiology and NYU Cancer Institute, NYU School of Medicine, New York 10016, USA.
Tim MalcolmDepartment of Pathology, University of Cambridge, CB2 0QQ Cambridge, UK.
Suzanne D TurnerDepartment of Pathology, University of Cambridge, CB2 0QQ Cambridge, UK.
Andrea HaitelClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Martin SusaniClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Ali MoazzamiDepartment of Chemistry and Biotechnology, Swedish University of Agricultural Sciences, 75007 Uppsala, Sweden.
Stefan Rose-JohnInstitute of Biochemistry, University of Kiel, 24098 Kiel, Germany.
Fritz AbergerDepartment of Molecular Biology, Paris-Lodron University of Salzburg, 5020 Salzburg, Austria.
Olaf MerkelClinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Richard Moriggl1] Ludwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria [2] Unit for Translational Methods in Cancer Research, University of Veterinary Medicine Vienna, 1210 Vienna, Austria.
Zoran CuligDepartment of Urology, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Helmut DolznigInstitute of Medical Genetics, Medical University of Vienna, 1090 Vienna, Austria.
Lukas Kenner1] Ludwig Boltzmann Institute for Cancer Research, Waehringerstrasse 13A, 1090 Vienna, Austria [2] Clinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria [3] Unit of Pathology of Laboratory Animals (UPLA), University of Veterinary Medicine Vienna, 1210 Vienna, Austria.
Medical University of Vienna · ATLudwig Boltzmann Institute for Cancer Research · ATKiel University · DENew York University · USQueen's University Belfast · GBUniversity of Cambridge · GBUniversity of Salzburg · ATUniversity of Tübingen · DEUniversity of Veterinary Medicine Vienna · ATAustrian Academy of Sciences · ATComprehensive Cancer Center Vienna · ATInnsbruck Medical University · ATJohannes Gutenberg University Mainz · DESwedish University of Agricultural Sciences · SEUniversity of Turin · ITUniversity of Ulster · GB
Funding
Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1MAustrian Science Fund FWF P 24428Austrian Science Fund FWF P 25629Austrian Science Fund FWF P 26011Austrian Science Fund FWF P 27616NCI NIH HHS P30 CA016087
Abstract
Prostate cancer (PCa) is the most prevalent cancer in men. Hyperactive STAT3 is thought to be oncogenic in PCa. However, targeting of the IL-6/STAT3 axis in PCa patients has failed to provide therapeutic benefit. Here we show that genetic inactivation of Stat3 or IL-6 signalling in a Pten-deficient PCa mouse model accelerates cancer progression leading to metastasis. Mechanistically, we identify p19(ARF) as a direct Stat3 target. Loss of Stat3 signalling disrupts the ARF-Mdm2-p53 tumour suppressor axis bypassing senescence. Strikingly, we also identify STAT3 and CDKN2A mutations in primary human PCa. STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases. In accordance, loss of STAT3 and p14(ARF) expression in patient tumours correlates with increased risk of disease recurrence and metastatic PCa. Thus, STAT3 and ARF may be prognostic markers to stratify high from low risk PCa patients. Our findings challenge the current discussion on therapeutic benefit or risk of IL-6/STAT3 inhibition.
Indexed as
AnimalsCell LineCyclin-Dependent Kinase Inhibitor p16Disease ProgressionGenes, p16HumansInterleukin-6MaleMiceMice, TransgenicNeoplasms, ExperimentalProstatic NeoplasmsProto-Oncogene Proteins c-mdm2PTEN PhosphohydrolaseSTAT3 Transcription FactorTumor Suppressor Protein p53Cdkn2a protein, mouseCyclin-Dependent Kinase Inhibitor p16Interleukin-6interleukin-6, mouseMdm2 protein, mouseProto-Oncogene Proteins c-mdm2PTEN PhosphohydrolasePten protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTumor Suppressor Protein p53
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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.