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Curcumin-Induced Apoptotic Cell Death in Human Glioma Cells Is Enhanced by Clusterin Deficiency

The result's identifiers

  • Result code in 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>

  • Result on the web

    <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>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Curcumin-Induced Apoptotic Cell Death in Human Glioma Cells Is Enhanced by Clusterin Deficiency

  • Original language description

    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&apos;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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

  • Continuities

    S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2025

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Pharmaceutics

  • ISSN

    1999-4923

  • e-ISSN

    1999-4923

  • Volume of the periodical

    17

  • Issue of the periodical within the volume

    6

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    19

  • Pages from-to

    679

  • UT code for WoS article

    001515050000001

  • EID of the result in the Scopus database

    2-s2.0-105009252504