Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2025 Nov;175(2):789-799.
doi: 10.1007/s11060-025-05176-w. Epub 2025 Jul 24.

Combined effects of escitalopram and vitamin E on phoenixin-20 secretion and neuroregulatory mechanisms in glioblastoma cells: a neuro-nutritional perspective

İrem Aydemir  1 , Gizem Tutkun  2 , Esra Tanyel Akcit  3 , Orhan Kocak  4 , Altinay Altinkaynak  1 , Kubra Yildirim  1   2 , Ece Simsek  5   6 , Ahmet Yilmaz Coban  1   2
Affiliations

Combined effects of escitalopram and vitamin E on phoenixin-20 secretion and neuroregulatory mechanisms in glioblastoma cells: a neuro-nutritional perspective

İrem Aydemir et al. J Neurooncol. 2025 Nov.

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.

Keywords: Escitalopram; GPR-173; Glioblastoma; Molecular docking; Phoenixin-20; Vitamin E.

PubMed Disclaimer

Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests.

References

    1. Wang D, Wang C, Wang L, Chen Y (2019) A comprehensive review in improving delivery of small-molecule chemotherapeutic agents overcoming the blood-brain/brain tumor barriers for glioblastoma treatment. Drug Deliv 26:551–565. https://doi.org/10.1080/10717544.2019.1616235 - DOI - PubMed - PMC
    1. Chang S-C, Shen W (2019) Antidepressant therapy in patients with cancer: A clinical review. Taiwan J Psychiatry 33:13. https://doi.org/10.4103/TPSY.TPSY_3_19 - DOI
    1. Pottegård A, García Rodríguez LA, Rasmussen L, Damkier P, Friis S, Gaist D (2016) Use of tricyclic antidepressants and risk of glioma: a nationwide case–control study. Br J Cancer 114:1265–1268. https://doi.org/10.1038/bjc.2016.109 - DOI - PubMed - PMC
    1. Kadasah SF, Alqahtani AMS, Alkhammash A, Radwan MO (2024) Beyond psychotropic: potential repurposing of Fluoxetine toward Cancer therapy. Int J Mol Sci 25:6314. https://doi.org/10.3390/ijms25126314 - DOI - PubMed - PMC
    1. Liu K-H, Yang S-T, Lin Y-K, Lin J-W, Lee Y-H, Wang J-Y et al (2015) Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis. Oncotarget 6:5088–5101. https://doi.org/10.18632/oncotarget.3243 - DOI - PubMed

MeSH terms

LinkOut - more resources