J 2024

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

MACEJOVA, Dana, Jakub KOLLAR, Pavel BOBÁĽ, Jan OTEVŘEL, Daniela SCHUSTER et. al.

Základní údaje

Originální název

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

Autoři

MACEJOVA, Dana (703 Slovensko), Jakub KOLLAR (203 Česká republika), Pavel BOBÁĽ (703 Slovensko, domácí), Jan OTEVŘEL (203 Česká republika, domácí), Daniela SCHUSTER (40 Rakousko) a Julius BRTKO (703 Slovensko)

Vydání

Molecular and Cellular Biochemistry, DORDRECHT, Springer, 2024, 0300-8177

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30104 Pharmacology and pharmacy

Stát vydavatele

Nizozemské království

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 4.300 v roce 2022

Organizační jednotka

Farmaceutická fakulta

UT WoS

001150933100001

Klíčová slova anglicky

Triorganotin isoselenocyanates; Retinoid X receptor; Apoptosis; Breast cancer

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 20. 5. 2024 14:42, Mgr. Daniela Černá

Anotace

V originále

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 mu M 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 mu M 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.