Curcumin-Induced Apoptotic Cell Death in Human Glioma Cells Is Enhanced by Clusterin Deficiency
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F25%3A10499227" target="_blank" >RIV/00216208:11310/25:10499227 - isvavai.cz</a>
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=608UK9g22n" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=608UK9g22n</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/pharmaceutics17060679" target="_blank" >10.3390/pharmaceutics17060679</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Curcumin-Induced Apoptotic Cell Death in Human Glioma Cells Is Enhanced by Clusterin Deficiency
Popis výsledku v původním jazyce
Background/Objectives: Glioblastoma is an aggressive brain tumor with limited treatment options and significant resistance to conventional therapies.Methods: In this study, we explored the effects of combining curcumin treatment with clusterin inhibition on cell death in glioma cells.Results: We observed that the combination of clusterin silencing and curcumin treatment induces cell death. This combination therapy significantly elevated reactive oxygen species (ROS), triggering oxidative stress, which acted as a key upstream mediator of apoptosis. Elevated ROS levels were found to be associated with caspase activation, suggesting apoptosis as the primary mode of cell death. Furthermore, autophagy was induced as a complementary mechanism, with upregulation of LC3B contributing to the enhanced cytotoxic effects.Conclusions: The synergy between clusterin knockdown-induced senescence and curcumin's pro-apoptotic and pro-autophagic effects highlights a potential novel therapeutic strategy for gliomas. These findings underscore the potential of this combination therapy in overcoming glioma resistance and improving treatment outcomes through the dual induction of oxidative stress and cell death pathways.
Název v anglickém jazyce
Curcumin-Induced Apoptotic Cell Death in Human Glioma Cells Is Enhanced by Clusterin Deficiency
Popis výsledku anglicky
Background/Objectives: Glioblastoma is an aggressive brain tumor with limited treatment options and significant resistance to conventional therapies.Methods: In this study, we explored the effects of combining curcumin treatment with clusterin inhibition on cell death in glioma cells.Results: We observed that the combination of clusterin silencing and curcumin treatment induces cell death. This combination therapy significantly elevated reactive oxygen species (ROS), triggering oxidative stress, which acted as a key upstream mediator of apoptosis. Elevated ROS levels were found to be associated with caspase activation, suggesting apoptosis as the primary mode of cell death. Furthermore, autophagy was induced as a complementary mechanism, with upregulation of LC3B contributing to the enhanced cytotoxic effects.Conclusions: The synergy between clusterin knockdown-induced senescence and curcumin's pro-apoptotic and pro-autophagic effects highlights a potential novel therapeutic strategy for gliomas. These findings underscore the potential of this combination therapy in overcoming glioma resistance and improving treatment outcomes through the dual induction of oxidative stress and cell death pathways.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30103 - Neurosciences (including psychophysiology)
Návaznosti výsledku
Projekt
—
Návaznosti
S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2025
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Pharmaceutics
ISSN
1999-4923
e-ISSN
1999-4923
Svazek periodika
17
Číslo periodika v rámci svazku
6
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
19
Strana od-do
679
Kód UT WoS článku
001515050000001
EID výsledku v databázi Scopus
2-s2.0-105009252504