S-allyl-cysteine triggers cytotoxic events in rat glioblastoma RG2 and C6 cells and improves the effect of temozolomide through the regulation of oxidative responses
Rattachement africain : mx, tr, es, ru, us. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Glioblastoma (GBM) is an aggressive form of cancer affecting the Central Nervous System (CNS) of thousands of people every year. Redox alterations have been shown to play a key role in the development and progression of these tumors as Reactive Oxygen Species (ROS) formation is involved in the modulation of several signaling pathways, transcription factors, and cytokine formation. The second-generation oral alkylating agent temozolomide (TMZ) is the first-line chemotherapeutic drug used to treat of GBM, though patients often develop primary and secondary resistance, reducing its efficacy. Antioxidants represent promising and potential coadjutant agents as they can reduce excessive ROS formation derived from chemo- and radiotherapy, while decreasing pharmacological resistance. S-allyl-cysteine (SAC) has been shown to inhibit the proliferation of several types of cancer cells, though its precise antiproliferative mechanisms remain poorly investigated. To date, SAC effects have been poorly explored in GBM cells. Here, we investigated the effects of SAC in vitro, either alone or in combination with TMZ, on several toxic and modulatory endpoints-including oxidative stress markers and transcriptional regulation-in two glioblastoma cell lines from rats, RG2 and C6, to elucidate some of the biochemical and cellular mechanisms underlying its antiproliferative properties. SAC (1-750 µM) decreased cell viability in both cell lines in a concentration-dependent manner, although C6 cells were more resistant to SAC at several of the tested concentrations. TMZ also produced a concentration-dependent effect, decreasing cell viability of both cell lines. In combination, SAC (1 µM or 100 µM) and TMZ (500 µM) enhanced the effects of each other. SAC also augmented the lipoperoxidative effect of TMZ and reduced cell antioxidant resistance in both cell lines by decreasing the TMZ-induced increase in the GSH/GSSG ratio. In RG2 and C6 cells, SAC per se had no effect on Nrf2/ARE binding activity, while in RG2 cells TMZ and the combination of SAC + TMZ decreased this activity. Our results demonstrate that SAC, alone or in combination with TMZ, exerts antitumor effects mediated by regulatory mechanisms of redox activity responses. SAC is also a safe drug for testing in other models as it produces non-toxic effects in primary astrocytes. Combined, these effects suggest that SAC affords antioxidant properties and potential antitumor efficacy against GBM.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- S-allyl-cysteine triggers cytotoxic events in rat glioblastoma RG2 and C6 cells and improves the effect of temozolomide through the regulation of oxidative responses
- Date Crossref
- 08/07/2024
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Universidad Nacional Autónoma de México pays non établi dans la noticeUniversité ou école supérieure
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Secretaria de Salud pays non établi dans la noticeOrganisme public
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Instituto Nacional de Pediatria Subdirección de Medicina Experimental pays non établi dans la noticeStructure de recherche
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Instituto Nacional de Cardiología Departamento de Biomedicina Cardiovascular pays non établi dans la noticeStructure de recherche
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Instituto Nacional de Neurología y Neurocirugía Departamento de Neuroquímica pays non établi dans la noticeStructure de recherche
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Gazi University pays non établi dans la noticeUniversité ou école supérieure
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Instituto Maimónides de Investigación Biomédica de Córdoba pays non établi dans la noticeStructure de recherche
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University of Córdoba pays non établi dans la noticeUniversité ou école supérieure
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Peoples' Friendship University of Russia and Department of Human Ecology and Bioelementology pays non établi dans la noticeUniversité ou école supérieure
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Sechenov University Laboratory of Molecular Dietetics pays non établi dans la noticeUniversité ou école supérieure
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Yaroslavl State University Laboratory of Molecular Ecobiomonitoring and Quality Control pays non établi dans la noticeUniversité ou école supérieure
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Albert Einstein College of Medicine Department of Molecular Pharmacology pays non établi dans la noticeUniversité ou école supérieure
Universidad Nacional Autónoma de México, Secretaria de Salud et Subdirección de Medicina Experimental — Instituto Nacional de Pediatria, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.