Evidence map›Paper›PMID 25671301›Full record

ArticleOncotarget2015

Fluoxetine, an antidepressant, suppresses glioblastoma by evoking AMPAR-mediated calcium-dependent apoptosis.

Kao-Hui Liu, Shun-Tai Yang, Yen-Kuang Lin, Jia-Wei Lin, Yi-Hsuan Lee, Jia-Yi Wang, Chaur-Jong Hu, En-Yuan Lin, Shu-Mei Chen, Chee-Kin Then and 1 more

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In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Kao-Hui LiuTaipei Medical University, College of Medicine, Graduate Institute of Medical Sciences, Taipei, Taiwan.
Shun-Tai YangTaipei Medical University-Shuang Ho Hospital, Department of Neurosurgery, Taipei, Taiwan.
Yen-Kuang LinTaipei Medical University, Biostatistics Center, Taipei, Taiwan.
Jia-Wei LinTaipei Medical University-Shuang Ho Hospital, Department of Neurosurgery, Taipei, Taiwan.
Yi-Hsuan LeeNational Yang-Ming University, Department and Institute of Physiology, Taipei, Taiwan.
Jia-Yi WangTaipei Medical University, College of Medicine, Graduate Institute of Medical Sciences, Taipei, Taiwan.
Chaur-Jong HuTaipei Medical University-Shuang Ho Hospital, School of Medicine, Department of Neurology, Taipei, Taiwan.
En-Yuan LinTaipei Medical University Hospital, Department of Neurosurgery, Taipei, Taiwan.
Shu-Mei ChenTaipei Medical University-Wan Fang Hospital, Department of Neurosurgery, Taipei, Taiwan.
Chee-Kin ThenTaipei Medical University, College of Medicine, School of Medicine, Taipei, Taiwan.
Shing-Chuan ShenTaipei Medical University, College of Medicine, Graduate Institute of Medical Sciences, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The efficacy of glioblastoma chemotherapy is not satisfactory; therefore, a new medication is expected to improve outcomes. As much evidence shows that antidepressants decrease cancer incidence and improve patients' quality of life, we therefore attempted to explore the potential for fluoxetine to be used to treat GBM and its possible underlying mechanism. The expression level of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) was determined using immunohistochemical staining and PCR analysis. The mechanism of fluoxetine-induced apoptosis of gliomas was elucidated. Computer modeling and a binding assay were conducted to investigate the interaction of fluoxetine with the AMPAR. The therapeutic effect of fluoxetine was evaluated using an animal model. We found that fluoxetine directly bound to AMPAR, thus inducing transmembrane Ca²⁺ influx. The rise in the intracellular calcium concentration ([Ca²⁺]i) causes mitochondrial Ca²⁺ overload, thereby triggering apoptosis. AMPARs are excessively expressed in glioma tissues, suggesting that fluoxetine specifically executes glioma cells. Our in vivo study revealed that fluoxetine suppressed the growth of glioblastomas in brains of Nu/Nu mice, an effect similar to that produced by temozolomide. Our preclinical studies suggest fluoxetine, a commonly used antidepressant, might be selectively toxic to gliomas and could provide a new approach for managing this disease.

Indexed as

AnimalsAntidepressive Agents, Second-GenerationApoptosisBrain NeoplasmsCalciumCell SurvivalFluoxetineGlioblastomaHumansMaleMiceMice, NudeMolecular Docking SimulationReceptors, GlutamateTreatment OutcomeXenograft Model Antitumor Assaysalpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, humanAntidepressive Agents, Second-GenerationCalciumFluoxetineReceptors, GlutamateAMPA receptorantidepressantexcitotoxicityglioblastoma

Identifiers

PMID25671301
PMCPMC4467135

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.