Combined effects of escitalopram and vitamin E on phoenixin-20 secretion and neuroregulatory mechanisms in glioblastoma cells: a neuro-nutritional perspective.
Journal of neuro-oncology, vol.175, no.2, pp.789-799, 2025 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 175 Issue: 2
- Publication Date: 2025
- Doi Number: 10.1007/s11060-025-05176-w
- Journal Name: Journal of neuro-oncology
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Page Numbers: pp.789-799
- Keywords: Escitalopram, Glioblastoma, GPR-173, Molecular docking, Phoenixin-20, Vitamin E
- Akdeniz University Affiliated: Yes
Abstract
Objective: Glioblastoma multiforme (GBM) is one of the most aggressive brain tumors, characterized by limited treatment options due to the blood-brain barrier and drug resistance. Escitalopram (Citoles), a selective serotonin reuptake inhibitor (SSRI), has recently attracted attention for its potential anti-tumor properties. This study aimed to evaluate the effects of Citoles and vitamin E on GBM cell viability, Phoenixin-20 (PNX-20) secretion, and their molecular interaction with the GPR-173 receptor. Methods: U87-MG glioblastoma cells were treated with various concentrations of Citoles and vitamin E, both individually and in combination. Cell viability was assessed using Trypan Blue exclusion and MTT assays. PNX-20 secretion was quantified via ELISA, and the binding potential of the compounds with GPR-173 was examined through in silico molecular docking analysis. Results: The combination treatment significantly reduced cell viability. ELISA results indicated that PNX-20 secretion increased markedly at 48 and 72 h post-treatment. Molecular docking analysis revealed that both compounds exhibited high binding affinity to the GPR-173 receptor, supporting their potential mechanisms of action. Conclusion: The combined use of Citoles and vitamin E demonstrated antiproliferative effects on GBM cells and significantly enhanced PNX-20 secretion, suggesting a meaningful neuropeptidergic response. These findings highlight the therapeutic potential of SSRIs in bridging neuroregulation and cancer biology.