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Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma
Approximately half of surgically-treated patients with low-grade-glioma (LGG) suffer recurrence or metastasis. Currently there is no effective drug treatment. While the selective COX-2 inhibitor celecoxib showed anti-neoplastic activity against several malignant tumors, its effects against LGG remai...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6763415/ https://www.ncbi.nlm.nih.gov/pubmed/28283800 http://dx.doi.org/10.1007/s11060-017-2380-5 |
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author | Sato, Aya Mizobuchi, Yoshifumi Nakajima, Kohei Shono, Kenji Fujihara, Toshitaka Kageji, Teruyoshi Kitazato, Keiko Matsuzaki, Kazuhito Mure, Hideo Kuwayama, Kazuyuki Sumi, Akiko Saya, Hideyuki Sampetrean, Oltea Nagahirao, Shinji |
author_facet | Sato, Aya Mizobuchi, Yoshifumi Nakajima, Kohei Shono, Kenji Fujihara, Toshitaka Kageji, Teruyoshi Kitazato, Keiko Matsuzaki, Kazuhito Mure, Hideo Kuwayama, Kazuyuki Sumi, Akiko Saya, Hideyuki Sampetrean, Oltea Nagahirao, Shinji |
author_sort | Sato, Aya |
collection | PubMed |
description | Approximately half of surgically-treated patients with low-grade-glioma (LGG) suffer recurrence or metastasis. Currently there is no effective drug treatment. While the selective COX-2 inhibitor celecoxib showed anti-neoplastic activity against several malignant tumors, its effects against LGG remain to be elucidated. Ours is the first report that the expression level of COX-2 in brain tissue samples from patients with LGG and in LGG cell lines is higher than in the non-neoplastic region and in normal brain cells. We found that celecoxib attenuated LGG cell proliferation in a dose-dependent manner. It inhibited the generation of prostaglandin E2 and induced apoptosis and cell-cycle arrest. We also show that celecoxib hampered the activation of the Akt/survivin- and the Akt/ID3 pathway in LGGs. These findings suggest that celecoxib may have a promising therapeutic potential and that the early treatment of LGG patients with the drug may be beneficial. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11060-017-2380-5) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6763415 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-67634152019-10-07 Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma Sato, Aya Mizobuchi, Yoshifumi Nakajima, Kohei Shono, Kenji Fujihara, Toshitaka Kageji, Teruyoshi Kitazato, Keiko Matsuzaki, Kazuhito Mure, Hideo Kuwayama, Kazuyuki Sumi, Akiko Saya, Hideyuki Sampetrean, Oltea Nagahirao, Shinji J Neurooncol Laboratory Investigation Approximately half of surgically-treated patients with low-grade-glioma (LGG) suffer recurrence or metastasis. Currently there is no effective drug treatment. While the selective COX-2 inhibitor celecoxib showed anti-neoplastic activity against several malignant tumors, its effects against LGG remain to be elucidated. Ours is the first report that the expression level of COX-2 in brain tissue samples from patients with LGG and in LGG cell lines is higher than in the non-neoplastic region and in normal brain cells. We found that celecoxib attenuated LGG cell proliferation in a dose-dependent manner. It inhibited the generation of prostaglandin E2 and induced apoptosis and cell-cycle arrest. We also show that celecoxib hampered the activation of the Akt/survivin- and the Akt/ID3 pathway in LGGs. These findings suggest that celecoxib may have a promising therapeutic potential and that the early treatment of LGG patients with the drug may be beneficial. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11060-017-2380-5) contains supplementary material, which is available to authorized users. Springer US 2017-03-10 2017 /pmc/articles/PMC6763415/ /pubmed/28283800 http://dx.doi.org/10.1007/s11060-017-2380-5 Text en © Springer Science+Business Media New York 2017 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 Sato, Aya Mizobuchi, Yoshifumi Nakajima, Kohei Shono, Kenji Fujihara, Toshitaka Kageji, Teruyoshi Kitazato, Keiko Matsuzaki, Kazuhito Mure, Hideo Kuwayama, Kazuyuki Sumi, Akiko Saya, Hideyuki Sampetrean, Oltea Nagahirao, Shinji Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title | Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title_full | Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title_fullStr | Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title_full_unstemmed | Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title_short | Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma |
title_sort | blocking cox-2 induces apoptosis and inhibits cell proliferation via the akt/survivin- and akt/id3 pathway in low-grade-glioma |
topic | Laboratory Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6763415/ https://www.ncbi.nlm.nih.gov/pubmed/28283800 http://dx.doi.org/10.1007/s11060-017-2380-5 |
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