ArticleCancer control : journal of the Moffitt Cancer Center
Tricyclic Antidepressants Modulate Stressed Mitochondria in Glioblastoma Multiforme Cells.
Article in Cancer control : journal of the Moffitt Cancer Center. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Repurposing neurological drugs for brain cancer therapeutics: A systematic approach to identify charged molecules for affinity-based local drug delivery systems.International journal of pharmaceutics · 2025Pooled it
- Two faces of Amitriptyline in anMolecular and clinical oncology · 2026Article
- Dissecting the Dual Drug Candidates Against Glioblastoma and Oligodendroglioma Through Integrated Transcriptome Analysis and Virtual Screening.Cell biochemistry and biophysics · 2025Article
- Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review.Cells · 2025Review
- NLRP3 inflammasome: structure, mechanism, drug-induced organ toxicity, therapeutic strategies, and future perspectives.RSC medicinal chemistry · 2025Review
- Mito-Modulatory Medication Use and Skeletal Muscle Bioenergetics Among Older Men and Women: The Study of Muscle, Mobility, and Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Repurposing Antidepressants and Phenothiazine Antipsychotics as Efflux Pump Inhibitors in Cancer and Infectious Diseases.Antibiotics (Basel, Switzerland) · 2023Review
- Agomelatine, Ketamine and Vortioxetine Attenuate Energy Cell Metabolism-In Vitro Study.International journal of molecular sciences · 2022Article
- Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management.Journal of hematology & oncology · 2022Review
- Review
- HTR1A Inhibits the Progression of Triple-Negative Breast Cancer via TGF-β Canonical and Noncanonical Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Repurposing of Anticancer Stem Cell Drugs in Brain Tumors.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Review
- Antidepressant drug use in glioblastoma patients: an epidemiological view.Neuro-oncology practice · 2020Article
- Induction of apoptosis through extrinsic/intrinsic pathways and suppression of ERK/NF-κB signalling participate in anti-glioblastoma of imipramine.Journal of cellular and molecular medicine · 2020Article
- Identification of a Metabolism-Related Risk Signature Associated With Clinical Prognosis in Glioblastoma Using Integrated Bioinformatic Analysis.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common feature of solid tumors, including glioblastoma multiforme (GBM), is mitochondrial dysfunction. However, it is reported that the current standard of anti-GBM therapies may potentiate mitochondrial damage and, in effect, support the aggressive character of cancer. As mitochondria are implicated in the modulation of cellular drug sensitivity and chemoresistance mechanisms, activation-stressed mitochondria in GBM cells may represent a new target for anti-GBM therapy that is nontoxic for normal cells.
methodsAs mitochondria are possible targets for antidepressant drugs used as adjuvant therapy in patients with GBM, we examined their influence on mitochondrial volume and activity, reactive oxygen species level, extracellular lactate concentration, and p65 NF-κB gene expression in GBM cells.
resultsOur investigation showed, for the first time, that tricyclic antidepressants, imipramine and amitriptyline, partially reverse GBM abnormalities.
conclusionIn the light of reported studies, the mitochondrial disturbance observed in glioma cells is a dynamic process that can be reversed or silenced. Moreover, imipramine and amitriptyline are attractive cellular metabolic modulators and can potentially be used to restoring a proper function of mitochondria in GBM cells.
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