• Je něco špatně v tomto záznamu ?

NOX1 and NOX2: Two enzymes that promote endothelial-to-mesenchymal transition induced by melanoma conditioned media

V. Platel, D. Lechevalier, C. Bourreau, S. Renault, I. Šoborová, C. Jeannière, L. Martin, O. Hérault, I. Corre, N. Clere

. 2022 ; 177 (-) : 106097. [pub] 20220124

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc22019331

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®. 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-β2 + /- IL-1β 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® 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.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc22019331
003      
CZ-PrNML
005      
20220804135553.0
007      
ta
008      
220720s2022 ne f 000 0|eng||
009      
AR
024    7_
$a 10.1016/j.phrs.2022.106097 $2 doi
035    __
$a (PubMed)35085755
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a ne
100    1_
$a Platel, Valentin $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France
245    10
$a NOX1 and NOX2: Two enzymes that promote endothelial-to-mesenchymal transition induced by melanoma conditioned media / $c V. Platel, D. Lechevalier, C. Bourreau, S. Renault, I. Šoborová, C. Jeannière, L. Martin, O. Hérault, I. Corre, N. Clere
520    9_
$a 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®. 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-β2 + /- IL-1β 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® 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.
650    _2
$a proliferace buněk $7 D049109
650    _2
$a kultivační média speciální $x farmakologie $7 D017077
650    12
$a endoteliální buňky $7 D042783
650    _2
$a epitelo-mezenchymální tranzice $7 D058750
650    _2
$a lidé $7 D006801
650    12
$a melanom $7 D008545
650    _2
$a reaktivní formy kyslíku $7 D017382
650    _2
$a nádorové mikroprostředí $7 D059016
655    _2
$a časopisecké články $7 D016428
700    1_
$a Lechevalier, Diane $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France; Department of Dermatology, Angers University Hospital, Angers, France
700    1_
$a Bourreau, Clara $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France
700    1_
$a Renault, Sarah $u PhyOS, UMR 1238, Inserm, Université de Nantes, Nantes, France
700    1_
$a Šoborová, Ivana $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France; Faculty of Pharmacy, Charles University, Hradec Králové, Czech Republic
700    1_
$a Jeannière, Caroline $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France
700    1_
$a Martin, Ludovic $u Department of Dermatology, Angers University Hospital, Angers, France
700    1_
$a Hérault, Olivier $u CNRS ERL 7001 LNOx and EA7501, University of Tours, Tours, France
700    1_
$a Corre, Isabelle $u Team SOAP, CRCINA, UMR 1232 Inserm, CNRS, Université de Nantes, Université d'Angers, Nantes, France
700    1_
$a Clere, Nicolas $u Univ Angers, Inserm, CNRS, MINT, SFR ICAT, Angers, France. Electronic address: nicolas.clere@univ-angers.fr
773    0_
$w MED00005744 $t Pharmacological research $x 1096-1186 $g Roč. 177, č. - (2022), s. 106097
856    41
$u https://pubmed.ncbi.nlm.nih.gov/35085755 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20220720 $b ABA008
991    __
$a 20220804135547 $b ABA008
999    __
$a ok $b bmc $g 1822788 $s 1170574
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2022 $b 177 $c - $d 106097 $e 20220124 $i 1096-1186 $m Pharmacological research $n Pharmacol Res $x MED00005744
LZP    __
$a Pubmed-20220720

Najít záznam

Citační ukazatele

Možnosti archivace