Evidence map›Paper›PMID 35259458›Full record

ArticleCancer letters2022

ETS-related gene (ERG) undermines genome stability in mouse prostate progenitors via Gsk3β dependent Nkx3.1 degradation.

Marco Lorenzoni, Dario De Felice, Giulia Beccaceci, Giorgia Di Donato, Veronica Foletto, Sacha Genovesi, Arianna Bertossi, Francesco Cambuli, Francesca Lorenzin, Aurora Savino and 14 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

24 authors at 6 institutions in 2 countries.

Marco LorenzoniDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Dario De FeliceDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Giulia BeccaceciDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Giorgia Di DonatoDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Veronica FolettoDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Sacha GenovesiDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Arianna BertossiDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Francesco CambuliDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Francesca LorenzinDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Aurora SavinoDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
Lidia AvalleDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
Alessia CimadamorePathological Anatomy, School of Medicine, United Hospitals, Polytechnic University of the Marche Region, Ancona, Italy.
Rodolfo MontironiMolecular Medicine and Cell Therapy Foundation, Polytechnic University of the Marche Region, Via Tronto, 10, Ancona, Italy.
Veronica WeberUnit of Surgical Pathology, Santa Chiara Hospital, Trento, Italy.
Francesco Giuseppe CarboneUnit of Surgical Pathology, Santa Chiara Hospital, Trento, Italy.
Mattia BarbareschiUnit of Surgical Pathology, Santa Chiara Hospital, Trento, Italy.
Francesca DemichelisDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Alessandro RomanelDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy.
Valeria PoliDepartment of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
Giannino Del SalUniversity of Trieste Department Life Sciences, ICGEB-Area Science Park Trieste, IFOM, Milan, Italy.
Marianna Kruithof-de JulioUrology Research Laboratory, Department for BioMedical Research DBMR, University of Bern, Bern, Switzerland; Translational Organoid Resource CORE, Department for BioMedical Research, University of Bern, Bern, Switzerland; Bern Center for Precision Medicine, Inselspital, University Hospital of Bern, Bern, Switzerland; Department of Urology, Inselspital, University Hospital of Bern, Bern, Switzerland.
Marco GaspariResearch Centre for Advanced Biochemistry and Molecular Biology, Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Catanzaro, Italy. Electronic address: gaspari@unicz.it.
Alessandro AlaimoDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy. Electronic address: alessandro.alaimo@unitn.it.
Andrea LunardiDepartment of Cellular, Computational and Integrative Biology-CIBIO, University of Trento, Trento, Italy. Electronic address: andrea.lunardi@unitn.it.
University of Trento · ITOspedale Santa Chiara · ITUniversity of Turin · ITMarche Polytechnic University · ITUniversity of Bern · CHUniversity of Trieste · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

21q22.2-3 deletion is the most common copy number alteration in prostate cancer (PCa). The genomic rearrangement results in the androgen-dependent de novo expression of ETS-related gene (ERG) in prostate cancer cells, a condition promoting tumor progression to advanced stages of the disease. Interestingly, ERG expression characterizes 5-30% of tumor precursor lesions - High Grade Prostatic Intraepithelial Neoplasia (HGPIN) - where its role remains unclear. Here, by combining organoids technology with Click-chemistry coupled Mass Spectrometry, we demonstrate a prominent role of ERG in remodeling the protein secretome of prostate progenitors. Functionally, by lowering autocrine Wnt-4 signaling, ERG represses canonical Wnt pathway in prostate progenitors, and, in turn, promotes the accumulation of DNA double strand breaks via Gsk3β-dependent degradation of the tumor suppressor Nkx3.1. On the other hand, by shaping extracellular paracrine signals, ERG strengthens the pro-oxidative transcriptional signature of inflammatory macrophages, which we demonstrate to infiltrate pre-malignant ERG positive prostate lesions. These findings highlight previously unrecognized functions of ERG in undermining adult prostate progenitor niche through cell autonomous and non-autonomous mechanisms. Overall, by supporting the survival and proliferation of prostate progenitors in the absence of growth stimuli and promoting the accumulation of DNA damage through destabilization of Nkx3.1, ERG could orchestrate the prelude to neoplastic transformation.

Indexed as

Glycogen Synthase Kinase 3 betaHomeodomain ProteinsProstateProstatic NeoplasmsTranscriptional Regulator ERGTranscription FactorsAnimalsGenomic InstabilityMaleMiceOncogene ProteinsTrans-ActivatorsERG protein, mouseGlycogen Synthase Kinase 3 betaGsk3b protein, mouseHomeodomain ProteinsNkx3-1 protein, mouseOncogene ProteinsTrans-ActivatorsTranscriptional Regulator ERGTranscription FactorsEgfERGNkx3.1OrganoidsProstateWnt

Identifiers

PMID35259458
PMCPMC8968219
OpenAlexW4220913982

What OpenQuestion holds

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Registered trials

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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.