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TGF-β induces matrisome pathological alterations and EMT in patient-derived prostate cancer tumoroids

S. Fernandes, J. Oliver-De La Cruz, S. Morazzo, F. Niro, M. Cassani, H. Ďuríková, A. Caravella, P. Fiore, G. Azzato, G. De Marco, A. Lauria, V. Izzi, V. Bosáková, J. Fric, P. Filipensky, G. Forte

. 2024 ; 125 (-) : 12-30. [pub] 20231108

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc24007806

Extracellular matrix (ECM) tumorigenic alterations resulting in high matrix deposition and stiffening are hallmarks of adenocarcinomas and are collectively defined as desmoplasia. Here, we thoroughly analysed primary prostate cancer tissues obtained from numerous patients undergoing radical prostatectomy to highlight reproducible structural changes in the ECM leading to the loss of the glandular architecture. Starting from patient cells, we established prostate cancer tumoroids (PCTs) and demonstrated they require TGF-β signalling pathway activity to preserve phenotypical and structural similarities with the tissue of origin. By modulating TGF-β signalling pathway in PCTs, we unveiled its role in ECM accumulation and remodelling in prostate cancer. We also found that TGF-β-induced ECM remodelling is responsible for the initiation of prostate cell epithelial-to-mesenchymal transition (EMT) and the acquisition of a migratory, invasive phenotype. Our findings highlight the cooperative role of TGF-β signalling and ECM desmoplasia in prompting prostate cell EMT and promoting tumour progression and dissemination.

Citace poskytuje Crossref.org

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$a Fernandes, Soraia $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic. Electronic address: Soraia.fernandes@fnusa.cz
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$a Extracellular matrix (ECM) tumorigenic alterations resulting in high matrix deposition and stiffening are hallmarks of adenocarcinomas and are collectively defined as desmoplasia. Here, we thoroughly analysed primary prostate cancer tissues obtained from numerous patients undergoing radical prostatectomy to highlight reproducible structural changes in the ECM leading to the loss of the glandular architecture. Starting from patient cells, we established prostate cancer tumoroids (PCTs) and demonstrated they require TGF-β signalling pathway activity to preserve phenotypical and structural similarities with the tissue of origin. By modulating TGF-β signalling pathway in PCTs, we unveiled its role in ECM accumulation and remodelling in prostate cancer. We also found that TGF-β-induced ECM remodelling is responsible for the initiation of prostate cell epithelial-to-mesenchymal transition (EMT) and the acquisition of a migratory, invasive phenotype. Our findings highlight the cooperative role of TGF-β signalling and ECM desmoplasia in prompting prostate cell EMT and promoting tumour progression and dissemination.
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$a Oliver-De La Cruz, Jorge $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic
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$a Morazzo, Sofia $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic; Faculty of Medicine, Department of Biomedical Sciences, Masaryk University, Brno 62500, Czech Republic
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$a Niro, Francesco $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic; Faculty of Medicine, Department of Biomedical Sciences, Masaryk University, Brno 62500, Czech Republic
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$a Cassani, Marco $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic
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$a Ďuríková, Helena $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic
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$a Caravella, Alessio $u Department of Computer Engineering, Modelling, Electronics and Systems Engineering (DIMES), University of Calabria (UNICAL), Via P. Bucci, Cubo 42C, Rende (CS) 87036, Italy
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$a Fiore, Piergiuseppe $u Department of Computer Engineering, Modelling, Electronics and Systems Engineering (DIMES), University of Calabria (UNICAL), Via P. Bucci, Cubo 42C, Rende (CS) 87036, Italy
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$a Azzato, Giulia $u Department of Computer Engineering, Modelling, Electronics and Systems Engineering (DIMES), University of Calabria (UNICAL), Via P. Bucci, Cubo 42C, Rende (CS) 87036, Italy
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$a De Marco, Giuseppe $u Information Technology Center (ICT), University of Calabria (UNICAL), Via P. Bucci, Cubo 22B, Rende (CS) 87036, Italy
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$a Lauria, Agostino $u Department of Engineering for Innovation, University of Salento (UNISALENTO), Corpo Z, Campus Ecotekne, SP.6 per Monteroni, Lecce (LE), Italy
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$a Izzi, Valerio $u Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu FI-90014, Finland; Faculty of Medicine, BioIM Research Unit, University of Oulu, Oulu FI-90014, Finland; Foundation for the Finnish Cancer Institute, Tukholmankatu 8, Helsinki, Finland
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$a Bosáková, Veronika $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic; Faculty of Medicine, Department of Biomedical Sciences, Masaryk University, Brno 62500, Czech Republic
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$a Fric, Jan $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic; Institute of Hematology and Blood Transfusion, Prague, Czech Republic
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$a Filipensky, Petr $u Department of Urology, St. Anne's University Hospital, Brno 60200, Czech Republic
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$a Forte, Giancarlo $u International Clinical Research Center, St. Anne's University Hospital, Brno 60200, Czech Republic; School of Cardiovascular and Metabolic Medicine & Sciences, King's College London, London SE5 9NU, UK. Electronic address: Giancarlo.forte@kcl.ac.uk
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