TY - JOUR
T1 - Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma
AU - Sato, Aya
AU - Mizobuchi, Yoshifumi
AU - Nakajima, Kohei
AU - Shono, Kenji
AU - Fujihara, Toshitaka
AU - Kageji, Teruyoshi
AU - Kitazato, Keiko
AU - Matsuzaki, Kazuhito
AU - Mure, Hideo
AU - Kuwayama, Kazuyuki
AU - Sumi, Akiko
AU - Saya, Hideyuki
AU - Sampetrean, Oltea
AU - Nagahirao, Shinji
N1 - Publisher Copyright:
© 2017, Springer Science+Business Media New York.
PY - 2017/4/1
Y1 - 2017/4/1
N2 - 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.
AB - 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.
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U2 - 10.1007/s11060-017-2380-5
DO - 10.1007/s11060-017-2380-5
M3 - Article
C2 - 28283800
AN - SCOPUS:85014749438
SN - 0167-594X
VL - 132
SP - 231
EP - 238
JO - Journal of Neuro-Oncology
JF - Journal of Neuro-Oncology
IS - 2
ER -
