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The effects of antiepileptic drugs on the growth of glioblastoma cell lines

To determine the effects of antiepileptic drug compounds on glioblastoma cellular growth, we exposed glioblastoma cell lines to select antiepileptic drugs. The effects of selected antiepileptic drugs on glioblastoma cells were measured by MTT assay. For compounds showing significant inhibition, cell...

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Autores principales: Lee, Ching-Yi, Lai, Hung-Yi, Chiu, Angela, Chan, She-Hung, Hsiao, Ling-Ping, Lee, Shih-Tseng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2016
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835521/
https://www.ncbi.nlm.nih.gov/pubmed/26758059
http://dx.doi.org/10.1007/s11060-016-2056-6
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author Lee, Ching-Yi
Lai, Hung-Yi
Chiu, Angela
Chan, She-Hung
Hsiao, Ling-Ping
Lee, Shih-Tseng
author_facet Lee, Ching-Yi
Lai, Hung-Yi
Chiu, Angela
Chan, She-Hung
Hsiao, Ling-Ping
Lee, Shih-Tseng
author_sort Lee, Ching-Yi
collection PubMed
description To determine the effects of antiepileptic drug compounds on glioblastoma cellular growth, we exposed glioblastoma cell lines to select antiepileptic drugs. The effects of selected antiepileptic drugs on glioblastoma cells were measured by MTT assay. For compounds showing significant inhibition, cell cycle analysis was performed. Statistical analysis was performed using SPSS. The antiepileptic compounds selected for screening included carbamazepine, ethosuximide, gabapentin, lamotrigine, levetiracetam, magnesium sulfate, oxcarbazepine, phenytoin, primidone, tiagabine, topiramate, valproic acid, and vigabatrin. Dexamethasone and temozolomide were used as a negative and positive control respectively. Our results showed temozolomide and oxcarbazepine significantly inhibited glioblastoma cell growth and reached IC(50) at therapeutic concentrations. The other antiepileptic drugs screened were unable to reach IC(50) at therapeutic concentrations. The metabolites of oxcarbazepine were also unable to reach IC(50.) Dexamethasone, ethosuximide, levetiracetam, and vigabatrin showed some growth enhancement though they did not reach statistical significance. The growth enhancement effects of ethosuximide, levetiracetam, and vigabatrin found in the study may indicate that these compounds should not be used for prophylaxis or short term treatment of epilepsy in glioblastoma. While valproic acid and oxcarbazepine were effective, the required dose of valproic acid was far above that used for the treatment of epilepsy and the metabolites of oxcarbazepine failed to reach significant growth inhibition ruling out the use of oral oxcarbazepine or valproic acid as monotherapy in glioblastoma. The possibility of using these compounds as local treatment is a future area of study.
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spelling pubmed-48355212016-05-04 The effects of antiepileptic drugs on the growth of glioblastoma cell lines Lee, Ching-Yi Lai, Hung-Yi Chiu, Angela Chan, She-Hung Hsiao, Ling-Ping Lee, Shih-Tseng J Neurooncol Laboratory Investigation To determine the effects of antiepileptic drug compounds on glioblastoma cellular growth, we exposed glioblastoma cell lines to select antiepileptic drugs. The effects of selected antiepileptic drugs on glioblastoma cells were measured by MTT assay. For compounds showing significant inhibition, cell cycle analysis was performed. Statistical analysis was performed using SPSS. The antiepileptic compounds selected for screening included carbamazepine, ethosuximide, gabapentin, lamotrigine, levetiracetam, magnesium sulfate, oxcarbazepine, phenytoin, primidone, tiagabine, topiramate, valproic acid, and vigabatrin. Dexamethasone and temozolomide were used as a negative and positive control respectively. Our results showed temozolomide and oxcarbazepine significantly inhibited glioblastoma cell growth and reached IC(50) at therapeutic concentrations. The other antiepileptic drugs screened were unable to reach IC(50) at therapeutic concentrations. The metabolites of oxcarbazepine were also unable to reach IC(50.) Dexamethasone, ethosuximide, levetiracetam, and vigabatrin showed some growth enhancement though they did not reach statistical significance. The growth enhancement effects of ethosuximide, levetiracetam, and vigabatrin found in the study may indicate that these compounds should not be used for prophylaxis or short term treatment of epilepsy in glioblastoma. While valproic acid and oxcarbazepine were effective, the required dose of valproic acid was far above that used for the treatment of epilepsy and the metabolites of oxcarbazepine failed to reach significant growth inhibition ruling out the use of oral oxcarbazepine or valproic acid as monotherapy in glioblastoma. The possibility of using these compounds as local treatment is a future area of study. Springer US 2016-01-13 2016 /pmc/articles/PMC4835521/ /pubmed/26758059 http://dx.doi.org/10.1007/s11060-016-2056-6 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Laboratory Investigation
Lee, Ching-Yi
Lai, Hung-Yi
Chiu, Angela
Chan, She-Hung
Hsiao, Ling-Ping
Lee, Shih-Tseng
The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title_full The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title_fullStr The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title_full_unstemmed The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title_short The effects of antiepileptic drugs on the growth of glioblastoma cell lines
title_sort effects of antiepileptic drugs on the growth of glioblastoma cell lines
topic Laboratory Investigation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835521/
https://www.ncbi.nlm.nih.gov/pubmed/26758059
http://dx.doi.org/10.1007/s11060-016-2056-6
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