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Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells

Glioma patients constitute the greatest percentage of depressed neoplasm patients. These patients often require antidepressant treatment, but the effect of antidepressant drugs on glioma cells requires further evaluation. In the present study, we evaluated the effect of trifluoperazine (TFP) on the...

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Autores principales: Wen, Yulin, Zhang, Yong, Li, Jinbang, Luo, Feng, Huang, Zhongxi, Liu, Kunping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773581/
https://www.ncbi.nlm.nih.gov/pubmed/29348654
http://dx.doi.org/10.1038/s41598-018-19413-y
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author Wen, Yulin
Zhang, Yong
Li, Jinbang
Luo, Feng
Huang, Zhongxi
Liu, Kunping
author_facet Wen, Yulin
Zhang, Yong
Li, Jinbang
Luo, Feng
Huang, Zhongxi
Liu, Kunping
author_sort Wen, Yulin
collection PubMed
description Glioma patients constitute the greatest percentage of depressed neoplasm patients. These patients often require antidepressant treatment, but the effect of antidepressant drugs on glioma cells requires further evaluation. In the present study, we evaluated the effect of trifluoperazine (TFP) on the proliferation and apoptosis of glioma cells. Transcriptomic and bioinformatics analysis results suggested that antidepressant drugs, especially TFP, may upregulate the drug-resistant ability of glioma cells. A low concentration of TFP upregulated the viability of glioma cells. Colony formation and EdU assays confirmed that TFP treatment accelerates glioma cell proliferation, but no significant difference was found in the cell cycle distribution of glioma cells after treatment with TFP or control. Flow cytometry and TUNEL staining results suggested that TFP treatment decreased apoptosis in glioma cells. In addition, TFP treatment downregulated the intracellular Ca(2+) concentration of glioma cells. In vivo experimental results indicated that TFP treatment promoted proliferation and reduced apoptosis in xenograft tumours in nude mice. Taken together, our results suggest that a low concentration of TFP promotes proliferation and reduces apoptosis in glioma cells both in vitro and in vivo. The potential harmful effects of antidepressant drugs on gliomas require further evaluation before their use in glioma patients.
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spelling pubmed-57735812018-01-26 Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells Wen, Yulin Zhang, Yong Li, Jinbang Luo, Feng Huang, Zhongxi Liu, Kunping Sci Rep Article Glioma patients constitute the greatest percentage of depressed neoplasm patients. These patients often require antidepressant treatment, but the effect of antidepressant drugs on glioma cells requires further evaluation. In the present study, we evaluated the effect of trifluoperazine (TFP) on the proliferation and apoptosis of glioma cells. Transcriptomic and bioinformatics analysis results suggested that antidepressant drugs, especially TFP, may upregulate the drug-resistant ability of glioma cells. A low concentration of TFP upregulated the viability of glioma cells. Colony formation and EdU assays confirmed that TFP treatment accelerates glioma cell proliferation, but no significant difference was found in the cell cycle distribution of glioma cells after treatment with TFP or control. Flow cytometry and TUNEL staining results suggested that TFP treatment decreased apoptosis in glioma cells. In addition, TFP treatment downregulated the intracellular Ca(2+) concentration of glioma cells. In vivo experimental results indicated that TFP treatment promoted proliferation and reduced apoptosis in xenograft tumours in nude mice. Taken together, our results suggest that a low concentration of TFP promotes proliferation and reduces apoptosis in glioma cells both in vitro and in vivo. The potential harmful effects of antidepressant drugs on gliomas require further evaluation before their use in glioma patients. Nature Publishing Group UK 2018-01-18 /pmc/articles/PMC5773581/ /pubmed/29348654 http://dx.doi.org/10.1038/s41598-018-19413-y Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wen, Yulin
Zhang, Yong
Li, Jinbang
Luo, Feng
Huang, Zhongxi
Liu, Kunping
Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title_full Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title_fullStr Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title_full_unstemmed Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title_short Low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
title_sort low concentration trifluoperazine promotes proliferation and reduces calcium-dependent apoptosis in glioma cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773581/
https://www.ncbi.nlm.nih.gov/pubmed/29348654
http://dx.doi.org/10.1038/s41598-018-19413-y
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