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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023736%3A_____%2F24%3A00013592" target="_blank" >RIV/00023736:_____/24:00013592 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/24:00081512 RIV/00216224:14110/24:00135447

Výsledek na webu

<a href="https://doi.org/10.1016/j.matbio.2023.11.001" target="_blank" >https://doi.org/10.1016/j.matbio.2023.11.001</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.matbio.2023.11.001" target="_blank" >10.1016/j.matbio.2023.11.001</a>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30205 - Hematology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Matrix biology

ISSN

0945-053X

e-ISSN

—

Svazek periodika

125

Číslo periodika v rámci svazku

January

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

19

Strana od-do

12-30

Kód UT WoS článku

001134198600001

EID výsledku v databázi Scopus

2-s2.0-85179472524