2018Zhonghua shiyan waike zazhiRequires access

The effect of celecoxib on the biological characteristics of glioma cells

Sijun Zhao, Ming Zhao, Xin Xu, Yu You, Chongren Wang

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Abstract

Objective To investigate the effect of celecoxib on glioma cell proliferation, apoptosis, migration and invasion ability. Methods Methyl thiazol tetrazolium (MTT) assay was used to detect glial tumor cell proliferation of U251, T98G, U87 after treatment with 0, 20, 40 or 60 μmol/L celecoxib for 24, 48, 72 or 96 h. Flow cytometry was used to detect cell apoptosis after treatment with 40 μmol/L celecoxib for 48 h. Cell scratch test was used to detect cell migration after treatment with 40 μmol/L celecoxib for 48 h. Transwell was used to detect cell invasion after treatment with 40 μmol/L celecoxib for 48 h. The expression levels of cyclooxygenase-2 (COX-2), B cell lymphoma/leukemia-2 (bcl-2), B cell lymphoma/leukemia-2 associated X protein (bax), matrix metalloproteinase (MMP)-9, MMP-2 in cells was detected by Western blotting. Results Celecoxib can inhibit the proliferation of glioma cells and there is no obvious inhibitory effect on normal astrocytoma. The inhibitory effect of Celecoxib on glioma cell proliferation was depended on the reaction time and drug concentration. The apoptosis rate of glioma cell after 40μmol/L celecoxib was higher than the control group, and the difference was significant [(3.17±0.16)% vs. (16.08±1.57)%, (3.17±0.16)% vs. (16.08±1.57)%, t=14.169, P=0.000]. The migration rate of glioma cell after treatment with 40 μmol/L celecoxib was lower than the control group, the difference was significant . The invasion ability of glioma cell after 40 μmol/L celecoxib was lower than the control group, the difference was significant [(100.00±5.26)% vs. (41.28±5.84)%, t=12.940, P=0.000]. Glioma cells after celecoxib treatment in COX-2, bcl-2, MMP-9, MMP-2 was significantly decreased than control group [(229.5±11.36) vs. (97.32±7.95), t=16.512, P=0.000]. The bax protein of Glioma cells after celecoxib treatmentwas significantly higher than control group (t1=19.696, P1=0.000; t2=17.774, P2=0.000; t3=12.970, P3=0.000; t4=10.569, P4=0.001). Conclusion Celecoxib can inhibit glioma cell proliferation, migration and invasion ability, and promote the apoptosis of glioma cells, the mechanism of which was related to COX-2, bcl-2, bax, MMP-9, MMP-2. Key words: Glioma; Proliferation; Apoptosis; Invasion; Celecoxib

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Objective To investigate the effect of celecoxib on glioma cell proliferation, apoptosis, migration and invasion ability. Methods Methyl thiazol tetrazolium (MTT) assay was used to detect glial tumor cell proliferation of U251, T98G, U87 after treatment with 0, 20, 40 or 60 μmol/L celecoxib for 24, 48, 72 or 96 h. Flow cytometry was used to detect cell apoptosis after treatment with 40 μmol/L celecoxib for 48 h. Cell scratch test was used to detect cell migration after treatment with 40 μmol/L celecoxib for 48 h. Transwell was used to detect cell invasion after treatment with 40 μmol/L celecoxib for 48 h. The expression levels of cyclooxygenase-2 (COX-2), B cell lymphoma/leukemia-2 (bcl-2), B cell lymphoma/leukemia-2 associated X protein (bax), matrix metalloproteinase (MMP)-9, MMP-2 in cells was detected by Western blotting. Results Celecoxib can inhibit the proliferation of glioma cells and there is no obvious inhibitory effect on normal astrocytoma. The inhibitory effect of Celecoxib on glioma cell proliferation was depended on the reaction time and drug concentration. The apoptosis rate of glioma cell after 40μmol/L celecoxib was higher than the control group, and the difference was significant [(3.17±0.16)% vs. (16.08±1.57)%, (3.17±0.16)% vs. (16.08±1.57)%, t=14.169, P=0.000]. The migration rate of glioma cell after treatment with 40 μmol/L celecoxib was lower than the control group, the difference was significant . The invasion ability of glioma cell after 40 μmol/L celecoxib was lower than the control group, the difference was significant [(100.00±5.26)% vs. (41.28±5.84)%, t=12.940, P=0.000]. Glioma cells after celecoxib treatment in COX-2, bcl-2, MMP-9, MMP-2 was significantly decreased than control group [(229.5±11.36) vs. (97.32±7.95), t=16.512, P=0.000]. The bax protein of Glioma cells after celecoxib treatmentwas significantly higher than control group (t1=19.696, P1=0.000; t2=17.774, P2=0.000; t3=12.970, P3=0.000; t4=10.569, P4=0.001). Conclusion Celecoxib can inhibit glioma cell proliferation, migration and invasion ability, and promote the apoptosis of glioma cells, the mechanism of which was related to COX-2, bcl-2, bax, MMP-9, MMP-2. Key words: Glioma; Proliferation; Apoptosis; Invasion; Celecoxib

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Available abstract

Objective To investigate the effect of celecoxib on glioma cell proliferation, apoptosis, migration and invasion ability. Methods Methyl thiazol tetrazolium (MTT) assay was used to detect glial tumor cell proliferation of U251, T98G, U87 after treatment with 0, 20, 40 or 60 μmol/L celecoxib for 24, 48, 72 or 96 h. Flow cytometry was used to detect cell apoptosis after treatment with 40 μmol/L celecoxib for 48 h. Cell scratch test was used to detect cell migration after treatment with 40 μmol/L celecoxib for 48 h. Transwell was used to detect cell invasion after treatment with 40 μmol/L celecoxib for 48 h. The expression levels of cyclooxygenase-2 (COX-2), B cell lymphoma/leukemia-2 (bcl-2), B cell lymphoma/leukemia-2 associated X protein (bax), matrix metalloproteinase (MMP)-9, MMP-2 in cells was detected by Western blotting. Results Celecoxib can inhibit the proliferation of glioma cells and there is no obvious inhibitory effect on normal astrocytoma. The inhibitory effect of Celecoxib on glioma cell proliferation was depended on the reaction time and drug concentration. The apoptosis rate of glioma cell after 40μmol/L celecoxib was higher than the control group, and the difference was significant [(3.17±0.16)% vs. (16.08±1.57)%, (3.17±0.16)% vs. (16.08±1.57)%, t=14.169, P=0.000]. The migration rate of glioma cell after treatment with 40 μmol/L celecoxib was lower than the control group, the difference was significant . The invasion ability of glioma cell after 40 μmol/L celecoxib was lower than the control group, the difference was significant [(100.00±5.26)% vs. (41.28±5.84)%, t=12.940, P=0.000]. Glioma cells after celecoxib treatment in COX-2, bcl-2, MMP-9, MMP-2 was significantly decreased than control group [(229.5±11.36) vs. (97.32±7.95), t=16.512, P=0.000]. The bax protein of Glioma cells after celecoxib treatmentwas significantly higher than control group (t1=19.696, P1=0.000; t2=17.774, P2=0.000; t3=12.970, P3=0.000; t4=10.569, P4=0.001). Conclusion Celecoxib can inhibit glioma cell proliferation, migration and invasion ability, and promote the apoptosis of glioma cells, the mechanism of which was related to COX-2, bcl-2, bax, MMP-9, MMP-2. Key words: Glioma; Proliferation; Apoptosis; Invasion; Celecoxib

Key concepts: Celecoxib, Glioma, Apoptosis, Flow cytometry, Cell growth, Cell, Chemistry, MTT assay

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