ABSTRACT Prostate cancer is a major global health concern with limited treatment options for advanced disease. Its heterogeneity challenges the identification of crucial driver genes

implicated in disease progression. Activating protein-1 (AP-1) transcription factor is associated with cancer since the first identification of its subunits, the proto-oncogenes JUN and FOS.

Whereas both _JUN_ and _FOS_ have been implicated in prostate cancer, this study provides the first functional evidence that _FOS_ acts as a tumor suppressor during prostate cancer

progression and invasion. Data mining revealed decreased _FOS_ expression in prostate cancer and a further downregulation in metastatic disease, consistent with _FOS_ expression in cell

Interestingly, enhanced Jun expression is observed in the murine prostatic intraepithelial neoplasia lacking Fos. CRISPR/Cas9-mediated knockout of _Jun_ combined with _Fos_ and _Pten_

deficiency diminishes the increased proliferation rate in vivo but not the ability to form invasive disease. Overall, we demonstrate that loss of Fos promotes disease progression from

clinical latent prostate cancer to advanced disease through accelerated proliferation and invasiveness, partly through Jun. Access through your institution Buy or subscribe This is a preview

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A TUMOR SUPPRESSOR IN PROSTATE CANCER PROGRESSION AND STEMNESS VIA TRANSCRIPTIONALLY ACTIVATING SPRY2 AND REGULATING MEK/ERK SIGNALING Article Open access 16 October 2023 UNVEILING RACK1: A

KEY REGULATOR OF THE PI3K/AKT PATHWAY IN PROSTATE CANCER DEVELOPMENT Article 13 November 2024 _MEIS1_ DOWN-REGULATION BY MYC MEDIATES PROSTATE CANCER DEVELOPMENT THROUGH ELEVATED _HOXB13_

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Scholar  Download references ACKNOWLEDGEMENTS We thank Mette Simonsen for assistance with PET/MRI scanning. This work was funded by Danish cancer society (R146-A9394 and R204-A12490),

Ministry of health (4-1612-236/7), AUFF NOVA (E-2o15-FLS-9-8), Dagmar Marshalls Fond, Einar Willumsens Mindelegat, Harboefonden, Helge Peetz og Verner og hustru Vilma Peetz legat, Raimond og

Dagmar Ringgåed-Bohns Fond, The Aarhus University Research Foundation, and Thora og Viggo Grove’s Mindelegat (all to MKT). EFW and LB are supported by the European Research Council (grant:

ERC‐AdG 2016 CSI‐Fun-741888 to EFW) and the Medical University of Vienna. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

Maria Riedel, Martin F. Berthelsen, Huiqiang Cai & Jakob Haldrup * Department of Clinical Medicine and Urology, Aarhus University Hospital, Aarhus, Denmark Michael Borre * Department of

Biomedicine, Aarhus University, Aarhus, Denmark Søren R. Paludan & Martin K. Thomsen * South Denmark hospital, Vejle, Denmark Henrik Hager * Department of Nuclear Medicine & PET

Centre, Aarhus University Hospital, Aarhus, Denmark Mikkel H. Vendelbo * Laboratory Genes and Disease, Department of Dermatology, Medical University of Vienna (MUV), Vienna, Austria Erwin F.

Wagner * Laboratory Genes and Disease, Department of Laboratory Medicine, Medical University of Vienna (MUV), Vienna, Austria Erwin F. Wagner & Latifa Bakiri * Aarhus Institute of

Advanced Studies (AIAS), Aarhus University, Aarhus, Denmark Martin K. Thomsen Authors * Maria Riedel View author publications You can also search for this author inPubMed Google Scholar *

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Riedel, M., Berthelsen, M.F., Cai, H. _et al._ In vivo CRISPR inactivation of Fos promotes prostate cancer progression by altering the associated AP-1 subunit Jun. _Oncogene_ 40, 2437–2447

(2021). https://doi.org/10.1038/s41388-021-01724-6 Download citation * Received: 10 December 2020 * Revised: 11 February 2021 * Accepted: 18 February 2021 * Published: 05 March 2021 * Issue

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