« Previous
Next »
International Journal of Radiation Oncology * Biology * Physics
Volume 75, Issue 1
, Pages 225-234
, 1 September 2009
Modulation of Ionizing Radiation-Induced G2 Arrest by Cyclooxygenase-2 and its Inhibitor Celecoxib
References
- . Primary response genes induced by growth factors and tumor promoters. Annu Rev Biochem. 1991;60:281–319
- . The role of cyclooxygenases in inflammation, cancer, and development. Oncogene. 1999;18:7908–7916
- . The role of cyclooxygenase-2 inhibitors in combined modality therapy. In: Choy H editors. Chemoradiation in cancer therapy. Totowa, NJ: Humana Press; 2003;p. 391–408
- A selective cyclooxygenase-2 inhibitor, NS-398, enhances the effect of radiation in vitro and in vivo preferentially on the cells that express cyclooxygenase-2. Clin Cancer Res. 2001;7:2998–3005
- Radiosensitivity enhancement by celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, via COX-2-dependent cell cycle regulation on human cancer cells expressing differential COX-2 levels. Cancer Res. 2005;65:9501–9509
- . Radiation and the G2 phase of the cell cycle. Radiat Res. 1998;150(Suppl. 5):S52–S59
- Cyclooxygenase-independent down-regulation of multidrug resistance-associated protein-1 expression by celecoxib in human lung cancer cells. Mol Cancer Ther. 2005;4:1358–1363
- Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication. Nature. 2006;444:638–642
- Two molecularly distinct G(2)/M checkpoints are induced by ionizing irradiation. Mol Cell Biol. 2002;22:1049–1059
- An overactivated ATR/CHK1 pathway is responsible for the prolonged G2 accumulation in irradiated AT cells. J Biol Chem. 2003;278:30869–30874
- . Radiation and the cell cycle, revisited. Cancer Metastasis Rev. 2004;23:209–225
- . Essential and dispensable roles of ATR in cell cycle arrest and genome maintenance. Genes Dev. 2003;17:615–628
- ATM, ATR and DNA-PK: Initiators of the cellular genotoxic stress responses. Carcinogenesis. 2003;24:1571–1580
- . The role of ATM and ATR in DNA damage-induced cell cycle control. Prog Cell Cycle Res. 2003;5:393–411
- ATM and ATR: Sensing DNA damage. World J Gastroenterol. 2004;10:155–160
- Enhancement of tumor response to gamma-radiation by an inhibitor of cyclooxygenase-2 enzyme. J Natl Cancer Inst. 1999;91:1501–1504
- Preferential enhancement of tumor radioresponse by a cyclooxygenase-2 inhibitor. Cancer Res. 2000;60:1326–1331
- Enhancement of intrinsic tumor cell radiosensitivity induced by a selective cyclooxygenase-2 inhibitor. Clin Cancer Res. 2000;6:2513–2520
- In vitro enhancement of tumor cell radiosensitivity by a selective inhibitor of cyclooxygenase-2 enzyme: Mechanistic considerations. Int J Radiat Oncol Biol Phys. 2002;54:886–894
- Pronounced radiosensitization of cultured human cancer cells by COX inhibitor under acidic microenvironment. Int J Radiat Oncol Biol Phys. 2002;53:1314–1318
- NS 398 radiosensitizes an HNSCC cell line by possibly inhibiting radiation-induced expression of COX-2. Int J Radiat Oncol Biol Phys. 2003;57:1405–1412
- Cyclooxygenase-2 inhibitor NS398 enhances antitumor effect of irradiation on hormone refractory human prostate carcinoma cells. J Urol. 2003;170:2036–2039
- Potentiation of tumor response to radiation or chemoradiation by selective cyclooxygenase-2 enzyme inhibitors. Int J Radiat Oncol Biol Phys. 2004;58:369–375
- DNA damage checkpoint control in cells exposed to ionizing radiation. Oncogene. 2003;22:5834–5847
- . ATM and ATR: Components of an integrated circuit. Cell Cycle. 2007;6:414–417
- Adaptation to the ionizing radiation-induced G2 checkpoint occurs in human cells and depends on checkpoint kinase 1 and Polo-like kinase 1 kinases. Cancer Res. 2006;66:10253–10257
- . Human cancer cells require ATR for cell cycle progression following exposure to ionizing radiation. Oncogene. 2007;26:2535–2542
- . Inhibitors of the G2 DNA damage checkpoint and their potential for cancer therapy. Prog Cell Cycle Res. 2003;5:423–430
- . Potentiation of DNA-damage-induced cytotoxicity by G2 checkpoint abrogators. Curr Med Chem Anticancer Agents. 2003;3:35–46
This work was supported by the National Cancer Center (Grant No. 0710380-2).
H.J.J. is currently at the Department of Neurosurgery and Molecular Oncology Research Institute, Tuffs Medical Center, Boston, MA.
Conflict of interest none.
PII: S0360-3016(09)00720-2
doi: 10.1016/j.ijrobp.2009.04.086
© 2009 Elsevier Inc. All rights reserved.
« Previous
Next »
International Journal of Radiation Oncology * Biology * Physics
Volume 75, Issue 1
, Pages 225-234
, 1 September 2009
