COX-2 in radiotherapy: A potential target for radioprotection and radiosensitization

Cheki, M. and Yahyapour, R. and Farhood, B. and Rezaeyan, A. and Shabeeb, D. and Amini, P. and Rezapoor, S. and Najafi, M. (2018) COX-2 in radiotherapy: A potential target for radioprotection and radiosensitization. Current Molecular Pharmacology, 11 (3). pp. 173-183.

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Abstract

Background: Each year, millions of people die from cancer. Radiotherapy is one of the main treatment strategies for cancer patients. Despite the beneficial roles of treatment with radiation, several side effects may threaten normal tissues of patients in the years after treatment. Discussion: Moreover, high incidences of second primary cancers may reduce therapeutic ratio of radiotherapy. The search for appropriate targets of radiosensitization of tumor cells as well as radioprotection of normal tissues is one of the most interesting aims in radiobiology. Cyclooxygenase-2 (COX-2), as an inflammatory mediator has attracted interests for both aims. COX-2 activity is associated with ROS production and inflammatory signs in normal tissues. These effects further amplify radiation toxicity in irradiated cells as well as adjacent cells through a phenomenon known as Bystander effect. Increased COX-2 expression in distant non-irradiated tissues causes oxidative DNA damage and elevated cancer risk. Moreover, in tumors, the activation of this enzyme can increase resistance of malignant cells to radiotherapy. Hence, the inhibition of COX-2 has been proposed for better therapeutic response and amelioration of normal tissues. Celecoxib is one of the most studied COX-2 inhibitor for radiosensitization and radioprotection, while some other inhibitors have shown interesting results. Conclusion: In this review, we describe the role of COX-2 in radiation normal tissue injury as well as irradiated bystander and non-targeted cells. In addition, mechanisms of COX-2 induced tumor resistance to radiotherapy and the potential role of COX-2 inhibition are discussed. © 2018 Bentham Science Publishers.

Item Type: Article
Additional Information: cited By 18
Uncontrolled Keywords: 4 5 (4 chlorophenyl) 3 trifluoromethyl 1h pyrazol 1 ylbenzenesulfonamide; acetylsalicylic acid; celecoxib; cyclooxygenase 2; diclofenac; glutathione; ibuprofen; indometacin; interleukin 1; interleukin 6; malonaldehyde; meloxicam; monocyte chemotactic protein 1; n (2 cyclohexyloxy 4 nitrophenyl)methanesulfonamide; nimesulide; oxadiazole derivative; piroxicam; prostaglandin E2; protein kinase C alpha; RANTES; rofecoxib; superoxide dismutase; transforming growth factor beta receptor 1; triaryloxadiazole derivative; tumor necrosis factor; tumor necrosis factor alpha receptor; unclassified drug; cyclooxygenase 2; prostaglandin synthase inhibitor, apoptosis; breast cancer; cancer incidence; cancer resistance; cancer risk; cell infiltration; cellular distribution; disease severity; DNA damage; DNA repair; enzyme activation; enzyme active site; enzyme activity; enzyme binding; enzyme inhibition; esophageal squamous cell carcinoma; gamma radiation; human; ionizing radiation; mucosa inflammation; non small cell lung cancer; nonhuman; oxidative stress; paw edema; priority journal; protein expression; radiation dose; radiation exposure; radiation injury; radiation protection; radiosensitization; Review; second cancer; survival time; TGF beta signaling; treatment response; upregulation; uterine cervix carcinoma; bystander effect; drug effect; drug resistance; metabolism; radiation tolerance; radiotherapy, Bystander Effect; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Drug Resistance, Neoplasm; Humans; Radiation Tolerance; Radiotherapy
Subjects: Medicine
Pharmacology, Toxicology and Pharmaceutics
Divisions: Faculty of Para medicine > Department of Management Radiology and Medical Physics
Depositing User: ART . editor
Date Deposited: 10 Apr 2019 07:59
Last Modified: 10 Apr 2019 07:59
URI: http://eprints.kaums.ac.ir/id/eprint/4097

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