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Celecoxib, a cyclooxygenase-2 inhibitor, induces apoptosis in human osteosarcoma cell line MG-63 via down-regulation of PI3K/Akt.
Cell Biol Int. 2008 May; 32(5):494-501.CB

Abstract

Cyclooxygenase-2 (COX-2), involved in the inhibition of apoptosis and, the potentiation of cell growth, is frequently overexpressed in human malignancies including osteosarcoma (OS). We have attempted to identify the anti-proliferation of celecoxib, a selective COX-2 inhibitor, and the combination of celecoxib and cisplatin in MG-63 cells, and to explore the potential molecular mechanisms involved. MG-63 cells were treated with the combination of celecoxib and cisplatin or either agent alone for 48h in serum-supplemented medium. Celecoxib caused G1 phase arrest and significantly inhibited cell growth, as well as potentiating cisplatin-induced apoptosis. The effect was dose-dependent, and apoptotic changes such as DNA fragments and apoptotic bodies were observed. However, downregulation of COX-2 did not occur in cells treated with celecoxib. Phosphoinositide-3-kinase (PI3K)/Akt, survivin, bcl-2 were significantly downregulated in cells treated with the combination of celecoxib and cisplatin, and decreased survivin and bcl-2 levels were found in cells with wortmannin, a specific PI3K inhibitor. Moreover, the decreased expressions of procaspase-9, procaspase-3 and cleaved PARP-1 were detected by Western blot analysis. Therefore, celecoxib exerts its anti-tumor activities through COX-2-independent mechanisms, which may be PI3K/Akt-dependent, and survivin and bcl-2-related. PI3K may be at the center of the celecoxib effects, which play an essential role in the regulation of survivin and Bcl-2.

Authors+Show Affiliations

Department of Orthopedics, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, #88 Jie Fang Road, Hangzhou, 310009, Zhejiang, PR China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18078766

Citation

Liu, Bing, et al. "Celecoxib, a Cyclooxygenase-2 Inhibitor, Induces Apoptosis in Human Osteosarcoma Cell Line MG-63 Via Down-regulation of PI3K/Akt." Cell Biology International, vol. 32, no. 5, 2008, pp. 494-501.
Liu B, Shi ZL, Feng J, et al. Celecoxib, a cyclooxygenase-2 inhibitor, induces apoptosis in human osteosarcoma cell line MG-63 via down-regulation of PI3K/Akt. Cell Biol Int. 2008;32(5):494-501.
Liu, B., Shi, Z. L., Feng, J., & Tao, H. M. (2008). Celecoxib, a cyclooxygenase-2 inhibitor, induces apoptosis in human osteosarcoma cell line MG-63 via down-regulation of PI3K/Akt. Cell Biology International, 32(5), 494-501.
Liu B, et al. Celecoxib, a Cyclooxygenase-2 Inhibitor, Induces Apoptosis in Human Osteosarcoma Cell Line MG-63 Via Down-regulation of PI3K/Akt. Cell Biol Int. 2008;32(5):494-501. PubMed PMID: 18078766.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Celecoxib, a cyclooxygenase-2 inhibitor, induces apoptosis in human osteosarcoma cell line MG-63 via down-regulation of PI3K/Akt. AU - Liu,Bing, AU - Shi,Zhong-li, AU - Feng,Jie, AU - Tao,Hui-min, Y1 - 2007/11/05/ PY - 2007/05/06/received PY - 2007/08/12/revised PY - 2007/10/29/accepted PY - 2007/12/15/pubmed PY - 2008/8/9/medline PY - 2007/12/15/entrez SP - 494 EP - 501 JF - Cell biology international JO - Cell Biol Int VL - 32 IS - 5 N2 - Cyclooxygenase-2 (COX-2), involved in the inhibition of apoptosis and, the potentiation of cell growth, is frequently overexpressed in human malignancies including osteosarcoma (OS). We have attempted to identify the anti-proliferation of celecoxib, a selective COX-2 inhibitor, and the combination of celecoxib and cisplatin in MG-63 cells, and to explore the potential molecular mechanisms involved. MG-63 cells were treated with the combination of celecoxib and cisplatin or either agent alone for 48h in serum-supplemented medium. Celecoxib caused G1 phase arrest and significantly inhibited cell growth, as well as potentiating cisplatin-induced apoptosis. The effect was dose-dependent, and apoptotic changes such as DNA fragments and apoptotic bodies were observed. However, downregulation of COX-2 did not occur in cells treated with celecoxib. Phosphoinositide-3-kinase (PI3K)/Akt, survivin, bcl-2 were significantly downregulated in cells treated with the combination of celecoxib and cisplatin, and decreased survivin and bcl-2 levels were found in cells with wortmannin, a specific PI3K inhibitor. Moreover, the decreased expressions of procaspase-9, procaspase-3 and cleaved PARP-1 were detected by Western blot analysis. Therefore, celecoxib exerts its anti-tumor activities through COX-2-independent mechanisms, which may be PI3K/Akt-dependent, and survivin and bcl-2-related. PI3K may be at the center of the celecoxib effects, which play an essential role in the regulation of survivin and Bcl-2. SN - 1065-6995 UR - https://www.unboundmedicine.com/medline/citation/18078766/Celecoxib_a_cyclooxygenase_2_inhibitor_induces_apoptosis_in_human_osteosarcoma_cell_line_MG_63_via_down_regulation_of_PI3K/Akt_ L2 - https://doi.org/10.1016/j.cellbi.2007.10.008 DB - PRIME DP - Unbound Medicine ER -