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.

Basic information

Original name

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

Authors

MACEJOVA, Dana (703 Slovakia), Jakub KOLLAR (203 Czech Republic), Pavel BOBÁĽ (703 Slovakia, belonging to the institution), Jan OTEVŘEL (203 Czech Republic, belonging to the institution), Daniela SCHUSTER (40 Austria) and Julius BRTKO (703 Slovakia)

Edition

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

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30104 Pharmacology and pharmacy

Country of publisher

Netherlands

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 4.300 in 2022

Organization unit

Faculty of Pharmacy

DOI

UT WoS

001150933100001

Keywords in English

Triorganotin isoselenocyanates; Retinoid X receptor; Apoptosis; Breast cancer

Tags

Tags

International impact, Reviewed
Změněno: 20/5/2024 14:42, Mgr. Daniela Černá

Abstract

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.