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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...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2017
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.
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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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