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J Korean Soc Ther Radiol Oncol > Volume 21(3); 2003 > Article
The Journal of the Korean Society for Therapeutic Radiology and Oncology 2003;21(3): 216-221.
The Enhancement of Radiosensitivity by Celecoxib, Selective Cyclooxygenase-2 Inhibitor, on Human Cancer Cells Expressing Differential Levels of Cyclooxygenase-2
Hongryull Pyo, You Keun Shin, Hyun Seok Kim, Jinsil Seong, Chang Ok Suh, Gwi Eon Kim
1Lung Cancer Branch, Division of Common Cancer, National Cancer Center, Gyeonggi-Do, Korea. quasar93@ncc.re.kr
2Cancer Metastasis Research Center, Korea.
3Brain Korea 21 Project for Medical Science, Korea.
4Department of Radiation Oncology, Yonsei University, College of Medicine, Korea.
5Yonsei Cancer Center, Seoul, Korea.
To investigate the modulation of radiosensitivity by celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on cancer cells over- and under-expressing COX-2.
A clonogenic radiation survival analysis was performed on A549 human lung and MCF-7 human breast cancer cell lines incubated in both 1 and 10% fetal bovine serum (FBS) containing media. The apoptosis in both cell lines was measured after treatment with radiation and/or celecoxib.
Celecoxib enhanced the radiation sensitivity of the A549 cells in the medium containing the 10% FBS, with radiation enhancement ratios of 1.58 and 1.81 respectively, at surviving fractions of 0.1, with 30 microM and 50 microM celecoxib. This enhanced radiosensitivity disappeared in the medium containing the 1% FBS. Celecoxib did not change the radiation sensitivity of the MCF-7 cells in either media. The induction of apoptosis by celecoxib and radiation was not synergistic in either cell line.
Celecoxib, a selective COX-2 inhibitor, preferentially enhanced the effect of radiation on COX-2 over-expressing cancer cells compared to the cells with a low expression, and this effect disappeared on incubation of the cells during drug treatment in the medium with suboptimal serum concentration. Apoptosis did not appear to be the underlying mechanism of this radiation enhancement effect due to celecoxib on the A549 cells. These findings suggest radiosensitization by a selective COX-2 inhibitor is COX-2 dependent.
Key Words: Cyclooxygenase-2, COX-2, Radiation, A549, MCF-7
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