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Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma
Aberrant expression of MEG3 has been shown in various cancers. The purpose of this study is to evaluate the effect of MEG3 on glioma cells and the use of potential chemotherapeutics in glioma by modulating MEG3 expression. Cell viability, migration and chemosensitivity were assayed. Cell death was e...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10468657/ https://www.ncbi.nlm.nih.gov/pubmed/37525401 http://dx.doi.org/10.1111/jcmm.17883 |
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author | Degirmenci, Zehra Unver, Sena Kilic, Turker Avsar, Timucin |
author_facet | Degirmenci, Zehra Unver, Sena Kilic, Turker Avsar, Timucin |
author_sort | Degirmenci, Zehra |
collection | PubMed |
description | Aberrant expression of MEG3 has been shown in various cancers. The purpose of this study is to evaluate the effect of MEG3 on glioma cells and the use of potential chemotherapeutics in glioma by modulating MEG3 expression. Cell viability, migration and chemosensitivity were assayed. Cell death was evaluated in MEG3 overexpressing and MEG3 suppressed cells. MEG3 expression was compared in patient‐derived glioma cells concerning IDH1 mutation and WHO grades. Silencing of MEG3 inhibited cell proliferation and reduced cell migration while overexpression of MEG3 promoted proliferation in glioma cells. MEG3 inhibition improved the chemosensitivity of glioma cells to 5‐fluorouracil (5FU) but not to navitoclax. On the other hand, there is no significant effect of MEG3 expression on temozolamide (TMZ) treatment which is a standard chemotherapeutic agent in glioma. Suppression of the MEG3 gene in patient‐derived oligodendroglioma cells also showed the same effect whereas glioblastoma cell proliferation and chemosensitivity were not affected by MEG3 inhibition. Further, as a possible cell death mechanism of action apoptosis was investigated. Although MEG3 is a widely known tumour suppressor gene and its loss is associated with several cancer types, here we reported that MEG3 inhibition can be used for improving the efficiency of known chemotherapeutic drug sensitivity. We propose that the level of MEG3 should be evaluated in the treatment of different glioma subtypes that are resistant to effective drugs to increase the potential effective drug applications. |
format | Online Article Text |
id | pubmed-10468657 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-104686572023-09-01 Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma Degirmenci, Zehra Unver, Sena Kilic, Turker Avsar, Timucin J Cell Mol Med Original Articles Aberrant expression of MEG3 has been shown in various cancers. The purpose of this study is to evaluate the effect of MEG3 on glioma cells and the use of potential chemotherapeutics in glioma by modulating MEG3 expression. Cell viability, migration and chemosensitivity were assayed. Cell death was evaluated in MEG3 overexpressing and MEG3 suppressed cells. MEG3 expression was compared in patient‐derived glioma cells concerning IDH1 mutation and WHO grades. Silencing of MEG3 inhibited cell proliferation and reduced cell migration while overexpression of MEG3 promoted proliferation in glioma cells. MEG3 inhibition improved the chemosensitivity of glioma cells to 5‐fluorouracil (5FU) but not to navitoclax. On the other hand, there is no significant effect of MEG3 expression on temozolamide (TMZ) treatment which is a standard chemotherapeutic agent in glioma. Suppression of the MEG3 gene in patient‐derived oligodendroglioma cells also showed the same effect whereas glioblastoma cell proliferation and chemosensitivity were not affected by MEG3 inhibition. Further, as a possible cell death mechanism of action apoptosis was investigated. Although MEG3 is a widely known tumour suppressor gene and its loss is associated with several cancer types, here we reported that MEG3 inhibition can be used for improving the efficiency of known chemotherapeutic drug sensitivity. We propose that the level of MEG3 should be evaluated in the treatment of different glioma subtypes that are resistant to effective drugs to increase the potential effective drug applications. John Wiley and Sons Inc. 2023-07-31 /pmc/articles/PMC10468657/ /pubmed/37525401 http://dx.doi.org/10.1111/jcmm.17883 Text en © 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Degirmenci, Zehra Unver, Sena Kilic, Turker Avsar, Timucin Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title | Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title_full | Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title_fullStr | Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title_full_unstemmed | Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title_short | Silencing of the MEG3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
title_sort | silencing of the meg3 gene promoted anti‐cancer activity and drug sensitivity in glioma |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10468657/ https://www.ncbi.nlm.nih.gov/pubmed/37525401 http://dx.doi.org/10.1111/jcmm.17883 |
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