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Thymoquinone reversed doxorubicin resistance in U87 glioblastoma cells via targeting PI3K/Akt/mTOR signaling.
Shimia, Mohammad; Amini, Monireh; Ravari, Armin Ostovar; Tabnak, Peyman; Valizadeh, Amir; Ghaheri, Mohammad; Yousefi, Bahman.
Afiliación
  • Shimia M; Department of Neurosurgery, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Amini M; Department of Neurosurgery, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Ravari AO; Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Tabnak P; Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Valizadeh A; Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Ghaheri M; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
  • Yousefi B; Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Chem Biol Drug Des ; 104(2): e14587, 2024 Aug.
Article en En | MEDLINE | ID: mdl-39175102
ABSTRACT
Natural compounds such as thymoquinone (TQ) have recently gained increasing attention in treating glioblastoma (GBM). However, the effects of TQ in reversing drug resistance are not completely understood. Therefore, we aimed to examine TQ impacts on GBM cells with doxorubicin (DOX) resistance and the involvement of the PI3K/Akt/mTOR pathway. GBM cancer U87 and U87/DOX (resistant cells) cells were exposed to DOX and TQ, and cell proliferation was assessed by the MTT assay. ELISA was applied to evaluate cell apoptosis. The expression of apoptotic mediators such as Caspase-3, Bax, Bcl-2 and PI3K, Akt, mTOR, P-gp, and PTEN was assessed via qRT-PCR and western blot. We found that a combination of TQ and DOX suppressed dose-dependent cell growth capacity in cells and increased the cytotoxic effects of DOX in resistant cells. In addition, TQ treatment increased DOX-mediated apoptosis in U87/DOX cell lines via modulating the pro- and anti-apoptotic markers. A combination of TQ and DOX upregulated PTEN and downregulated PI3K, Akt, and mTOR, suppressing this signal transduction in resistant cells. In conclusion, we showed TQ potentiated doxorubicin-mediated antiproliferative and pro apoptotic function DOX-resistant glioblastoma cells, which is mediated by targeting and suppressing PI3K/Akt/mTOR signal transduction.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Doxorrubicina / Benzoquinonas / Apoptosis / Glioblastoma / Resistencia a Antineoplásicos / Fosfatidilinositol 3-Quinasas / Proteínas Proto-Oncogénicas c-akt / Serina-Treonina Quinasas TOR Límite: Humans Idioma: En Revista: Chem Biol Drug Des Asunto de la revista: BIOQUIMICA / FARMACIA / FARMACOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Doxorrubicina / Benzoquinonas / Apoptosis / Glioblastoma / Resistencia a Antineoplásicos / Fosfatidilinositol 3-Quinasas / Proteínas Proto-Oncogénicas c-akt / Serina-Treonina Quinasas TOR Límite: Humans Idioma: En Revista: Chem Biol Drug Des Asunto de la revista: BIOQUIMICA / FARMACIA / FARMACOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido