Proapoptotic and proautophagy effect of H1-receptor antagonist desloratadine in human glioblastoma cell lines

Glioblastomas are aggressive and usually incurable high-grade gliomas without adequate treatment. In this study, we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates. All experiments were performed on...

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Published in:	Medical oncology (Northwood, London, England) Vol. 40; no. 8; p. 241
Main Authors:	Vidicevic-Novakovic, Sasenka, Stanojevic, Zeljka, Tomonjic, Nina, Karapandza, Katarina, Zekovic, Janko, Martinovic, Tamara, Grujicic, Danica, Ilic, Rosanda, Raicevic, Savo, Tasic, Jelena, Isakovic, Aleksandra
Format:	Journal Article
Language:	English
Published:	New York Springer US 15-07-2023 Springer Nature B.V
Subjects:	AMP-Activated Protein Kinases Antineoplastic Agents - therapeutic use Apoptosis Autophagy Brain cancer Cell culture Cell Line, Tumor Cell Proliferation Cytotoxicity Glioblastoma - drug therapy Glioblastoma - metabolism Hematology Histamine Humans Internal Medicine Kinases Medical prognosis Medicine Medicine & Public Health Metabolism Nervous system Neurosurgery Oncology Original Paper Oxidative stress Pathology TOR Serine-Threonine Kinases - metabolism Tumors Oxidative stress Autophagy Glioblastoma Desloratadine Apoptosis
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Summary:	Glioblastomas are aggressive and usually incurable high-grade gliomas without adequate treatment. In this study, we aimed to investigate the potential of desloratadine to induce apoptosis/autophagy as genetically regulated processes that can seal cancer cell fates. All experiments were performed on U251 human glioblastoma cell line and primary human glioblastoma cell culture. Cytotoxic effect of desloratadine was investigated using MTT and CV assays, while oxidative stress, apoptosis, and autophagy were detected by flow cytometry and immunoblot. Desloratadine treatment decreased cell viability of U251 human glioblastoma cell line and primary human glioblastoma cell culture (IC50 value 50 µM) by an increase of intracellular reactive oxygen species and caspase activity. Also, desloratadine decreased the expression of main autophagy repressor mTOR and its upstream activator Akt and increased the expression of AMPK. Desloratadine exerted dual cytotoxic effect inducing both apoptosis- and mTOR/AMPK-dependent cytotoxic autophagy in glioblastoma cells and primary glioblastoma cell culture.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1559-131X 1357-0560 1559-131X
DOI:	10.1007/s12032-023-02117-3