Suppression of proliferation and activation of cell death by sodium selenite involves mitochondria and lysosomes in chemoresistant bladder cancer cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11150%2F19%3A10395465" target="_blank" >RIV/00216208:11150/19:10395465 - isvavai.cz</a>

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=WLpu2jWD_N" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=WLpu2jWD_N</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.jtemb.2018.11.009" target="_blank" >10.1016/j.jtemb.2018.11.009</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Suppression of proliferation and activation of cell death by sodium selenite involves mitochondria and lysosomes in chemoresistant bladder cancer cells

Popis výsledku v původním jazyce

The specific effects of sodium selenite (selenite) on a chemoresistant human bladder cancer cell line RT-112/D21 were investigated during 72 h. Selenite at low concentration of 2.5 mu mol (otherwise tolerated in normal urothelial cells UROtsa) suppressed growth and proliferation of the tested cancer cells via induced oxidative stress. Selenite further altered mitochondrial functions (i.e. decreased mitochondrial membrane potential, increased production of superoxide and reduced ATP synthesis), disrupted lysosomal membranes and activated autophagy. These changes in selenite-exposed cells ultimately resulted in their demise via necrosis and other cell death modality displaying heterotypic apoptotic and autophagic features.

Název v anglickém jazyce

Suppression of proliferation and activation of cell death by sodium selenite involves mitochondria and lysosomes in chemoresistant bladder cancer cells

Popis výsledku anglicky

The specific effects of sodium selenite (selenite) on a chemoresistant human bladder cancer cell line RT-112/D21 were investigated during 72 h. Selenite at low concentration of 2.5 mu mol (otherwise tolerated in normal urothelial cells UROtsa) suppressed growth and proliferation of the tested cancer cells via induced oxidative stress. Selenite further altered mitochondrial functions (i.e. decreased mitochondrial membrane potential, increased production of superoxide and reduced ATP synthesis), disrupted lysosomal membranes and activated autophagy. These changes in selenite-exposed cells ultimately resulted in their demise via necrosis and other cell death modality displaying heterotypic apoptotic and autophagic features.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Trace Elements in Medicine and Biology

ISSN

0946-672X

e-ISSN

—

Svazek periodika

52

Číslo periodika v rámci svazku

March

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

10

Strana od-do

58-67

Kód UT WoS článku

000463958300010

EID výsledku v databázi Scopus

2-s2.0-85057456554