Identifikační kód |
RIV/00216208:11160/22:10458658 |
Název v anglickém jazyce |
NOX1 and NOX2: Two enzymes that promote endothelial-to-mesenchymal transition induced by melanoma conditioned media |
Druh |
J - Recenzovaný odborný článek (Jimp, Jsc a Jost) |
Poddruh |
J/A - Článek v odborném periodiku je obsažen v databázi Web of Science společností Thomson Reuters s příznakem „Article“, „Review“ nebo „Letter“ (Jimp) |
Jazyk |
eng - angličtina |
Vědní obor |
30104 - Pharmacology and pharmacy |
Rok uplatnění |
2022 |
Kód důvěrnosti údajů |
S - Úplné a pravdivé údaje o výsledku nepodléhající ochraně podle zvláštních právních předpisů. |
Počet výskytů výsledku |
1 |
Popis výsledku v anglickém jazyce |
Tumor microenvironment plays an important role in melanoma progression. Recent studies reported endothelial cells (EC) are involved in endothelial-to-mesenchymal transition (EndMT). During this phenotypic switch, EC progressively lose their endothelial markers and acquire mesenchymal properties. Depending on their concentration, reactive oxygen species (ROS) can control tumor growth. In EC, ROS are mainly produced by NAPDH oxidases (NOX) such as NOX1 and NOX2. The aim of the present study was to determine the role of these enzymes in EndMT induced by conditioned media (CM) from SK-MEL 28 melanoma cells. The capacity of CM to induce EndMT in HUVEC after 24 h, 48 h or 72 h has been evaluated by following endothelial HUVECs proliferation, migration and their capacity to form capillary on ECMgel(R). Furthermore, EndMT was confirmed by western blot and flow cytometry. To determine the role of NOX in EndMT, specific NOX1 and/or NOX2 inhibitors has been tested. TGF-beta 2 +/- IL-1 beta was used as positive control. ROS production was determined through DCFDA assay. An altered endothelial phenotype was found in CM-treated HUVECs. This phenotypic modification was correlated with a decrease in both capillary formation on ECMgel(R) and cell proliferation and an increase in cell migration. Exposure to CM for 48 h significantly enhanced intracellular HUVECs ROS production and this increase was prevented by the dual pharmacological inhibition of NOX1 and NOX2. Furthermore, inhibition of NOX1/2 also leads to a partial reversion of CM-induced EndMT. These data confirmed the role of NOX1 and NOX2 in EndMT induced by melanoma cancer cell secretome. |
Klíčová slova oddělená středníkem |
NADPH oxidases;ROS;Melanoma;Endothelial-to-mesenchymal transition;Endothelial cell |
Stránka www, na které se nachází výsledek |
https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=1vuN8yyG57 |
DOI výsledku |
10.1016/j.phrs.2022.106097 |
Odkaz na údaje z výzkumu |
- |