Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Triphenyltin isoselenocyanate: a novel nuclear retinoid X receptor ligand with antiproliferative and cytotoxic properties in cell lines derived from human breast cancer

D. Macejova, J. Kollar, P. Bobal, J. Otevrel, D. Schuster, J. Brtko

. 2024 ; 479 (11) : 3091-3106. [pub] 20240116

Language English Country Netherlands

Document type Journal Article

Grant support
APVV-20-0314 Agentúra na Podporu Výskumu a Vývoja
APVV-15-0372 Agentúra na Podporu Výskumu a Vývoja
Vega 2/0116/21 Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
2019-10-15-009 Slovak Academic Information Agency
MUNI/A/1682/2020 Masarykova Univerzita

E-resources Online Full text

NLK ProQuest Central from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost) from 2011-01-01 to 1 year ago
Health & Medicine (ProQuest) from 1997-01-01 to 1 year ago

Several commercially available triorganotin compounds were previously found to function as agonist ligands for nuclear retinoid X receptor (RXR) molecules. Triphenyltin isoselenocyanate (TPT-NCSe), a novel selenium atom containing a derivative of triorganotin origin, was found to represent a new cognate bioactive ligand for RXRs. TPT-NCSe displayed a concentration- and time-dependent decrease in the cell viability in both human breast carcinoma MCF-7 (estrogen receptor positive) and MDA‐MB‐231 (triple negative) cell lines. Reactive oxygen species levels generated in response to TPT-NCSe were significantly higher in both carcinoma cell lines treated with TPT-NCSe when compared to mock-treated samples. Treatment with 500 nM TPT-NCSe caused a decrease in SOD1 and increased SOD2 mRNA in MCF-7 cells. The levels of SOD2 mRNA were more increased following the treatment with TPT-NCSe along with 1 μM all-trans retinoic acid (AtRA) in MCF-7 cells. An increased superoxide dismutase SOD1 and SOD2 mRNA levels were also detected in combination treatment of 500 nM TPT-NCSe and 1 μM AtRA in TPT-NCSe-treated MDA-MB-231 cells. The data have also shown that TPT-NCSe induces apoptosis via a caspase cascade triggered by the mitochondrial apoptotic pathway. TPT-NCSe modulates the expression levels of apoptosis‐related proteins, Annexin A5, Bcl‐2 and BAX family proteins, and finally, it enhances the expression levels of its cognate nuclear receptor subtypes RXRalpha and RXRbeta.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc25003751
003      
CZ-PrNML
005      
20250206104654.0
007      
ta
008      
250121s2024 ne f 000 0|eng||
009      
AR
024    7_
$a 10.1007/s11010-023-04914-w $2 doi
035    __
$a (PubMed)38227157
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a ne
100    1_
$a Macejova, Dana $u Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05, Bratislava, Slovak Republic. ueenmace@savba.sk $1 https://orcid.org/0000000297228612
245    10
$a Triphenyltin isoselenocyanate: a novel nuclear retinoid X receptor ligand with antiproliferative and cytotoxic properties in cell lines derived from human breast cancer / $c D. Macejova, J. Kollar, P. Bobal, J. Otevrel, D. Schuster, J. Brtko
520    9_
$a Several commercially available triorganotin compounds were previously found to function as agonist ligands for nuclear retinoid X receptor (RXR) molecules. Triphenyltin isoselenocyanate (TPT-NCSe), a novel selenium atom containing a derivative of triorganotin origin, was found to represent a new cognate bioactive ligand for RXRs. TPT-NCSe displayed a concentration- and time-dependent decrease in the cell viability in both human breast carcinoma MCF-7 (estrogen receptor positive) and MDA‐MB‐231 (triple negative) cell lines. Reactive oxygen species levels generated in response to TPT-NCSe were significantly higher in both carcinoma cell lines treated with TPT-NCSe when compared to mock-treated samples. Treatment with 500 nM TPT-NCSe caused a decrease in SOD1 and increased SOD2 mRNA in MCF-7 cells. The levels of SOD2 mRNA were more increased following the treatment with TPT-NCSe along with 1 μM all-trans retinoic acid (AtRA) in MCF-7 cells. An increased superoxide dismutase SOD1 and SOD2 mRNA levels were also detected in combination treatment of 500 nM TPT-NCSe and 1 μM AtRA in TPT-NCSe-treated MDA-MB-231 cells. The data have also shown that TPT-NCSe induces apoptosis via a caspase cascade triggered by the mitochondrial apoptotic pathway. TPT-NCSe modulates the expression levels of apoptosis‐related proteins, Annexin A5, Bcl‐2 and BAX family proteins, and finally, it enhances the expression levels of its cognate nuclear receptor subtypes RXRalpha and RXRbeta.
650    _2
$a lidé $7 D006801
650    12
$a organocínové sloučeniny $x farmakologie $7 D009947
650    12
$a nádory prsu $x farmakoterapie $x metabolismus $x patologie $7 D001943
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a MFC-7 buňky $7 D061986
650    _2
$a ligandy $7 D008024
650    _2
$a retinoidní X receptory $x metabolismus $7 D047488
650    _2
$a proliferace buněk $x účinky léků $7 D049109
650    _2
$a superoxiddismutasa 1 $x metabolismus $x genetika $7 D000072105
650    _2
$a superoxiddismutasa $x metabolismus $7 D013482
650    _2
$a apoptóza $x účinky léků $7 D017209
650    _2
$a nádorové buněčné linie $7 D045744
650    _2
$a reaktivní formy kyslíku $x metabolismus $7 D017382
650    _2
$a organoselenové sloučeniny $x farmakologie $x chemie $7 D016566
655    _2
$a časopisecké články $7 D016428
700    1_
$a Kollar, Jakub $u Department of Pharmaceutical and Medicinal Chemistry, Institute of Pharmacy, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria
700    1_
$a Bobal, Pavel $u Department of Chemical Drugs, Faculty of Pharmacy, Masaryk University, Palackého třída 1946/1, 612 00, Brno, Czech Republic
700    1_
$a Otevrel, Jan $u Department of Chemical Drugs, Faculty of Pharmacy, Masaryk University, Palackého třída 1946/1, 612 00, Brno, Czech Republic
700    1_
$a Schuster, Daniela $u Department of Pharmaceutical and Medicinal Chemistry, Institute of Pharmacy, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria
700    1_
$a Brtko, Julius $u Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05, Bratislava, Slovak Republic
773    0_
$w MED00003385 $t Molecular and cellular biochemistry $x 1573-4919 $g Roč. 479, č. 11 (2024), s. 3091-3106
856    41
$u https://pubmed.ncbi.nlm.nih.gov/38227157 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y - $z 0
990    __
$a 20250121 $b ABA008
991    __
$a 20250206104649 $b ABA008
999    __
$a ok $b bmc $g 2263495 $s 1239758
BAS    __
$a 3
BAS    __
$a PreBMC-MEDLINE
BMC    __
$a 2024 $b 479 $c 11 $d 3091-3106 $e 20240116 $i 1573-4919 $m Molecular and cellular biochemistry $n Mol Cell Biochem $x MED00003385
GRA    __
$a APVV-20-0314 $p Agentúra na Podporu Výskumu a Vývoja
GRA    __
$a APVV-15-0372 $p Agentúra na Podporu Výskumu a Vývoja
GRA    __
$a Vega 2/0116/21 $p Vedecká Grantová Agentúra MŠVVaŠ SR a SAV
GRA    __
$a 2019-10-15-009 $p Slovak Academic Information Agency
GRA    __
$a MUNI/A/1682/2020 $p Masarykova Univerzita
LZP    __
$a Pubmed-20250121

Find record

Citation metrics

Loading data ...

Archiving options

Loading data ...